Guyton and Hall Textbook of Medical Physiology

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Cleaned version with corrected pagination and bookmarks. Cover Note to Instructors Guyton and Hall Textbook of Medical Physiology Copyright Dedication Preface Unit I: Introduction to Physiology: The Cell and General Physiology Chapter 1: Functional Organization of the Human Body and Control of the “Internal Environment” Human Physiology CELLS ARE THE LIVING UNITS OF THE BODY Microorganisms Living in the Body Outnumber Human Cells EXTRACELLULAR FLUID—THE “INTERNAL ENVIRONMENT” Differences in Extracellular and Intracellular Fluids HOMEOSTASIS—MAINTENANCE OF A NEARLY CONSTANT INTERNAL ENVIRONMENT Homeostatic Compensations in Diseases EXTRACELLULAR FLUID TRANSPORT AND MIXING SYSTEM—THE BLOOD CIRCULATORY SYSTEM ORIGIN OF NUTRIENTS IN THE EXTRACELLULAR FLUID Respiratory System Gastrointestinal Tract Liver and Other Organs That Perform Primarily Metabolic Functions Musculoskeletal System REMOVAL OF METABOLIC END PRODUCTS Removal of Carbon Dioxide by the Lungs Kidneys Gastrointestinal Tract Liver REGULATION OF BODY FUNCTIONS Nervous System Hormone Systems PROTECTION OF THE BODY Immune System Integumentary System REPRODUCTION CONTROL SYSTEMS OF THE BODY EXAMPLES OF CONTROL MECHANISMS Regulation of Oxygen and Carbon Dioxide Concentrationsin the Extracellular Fluid Regulation of Arterial Blood Pressure Normal Ranges and Physical Characteristics of Important Extracellular Fluid Constituents CHARACTERISTICS OF CONTROL SYSTEMS Negative Feedback Nature of Most Control Systems Gain of a Control System Positive Feedback May Cause Vicious Cycles and Death Positive Feedback Can Sometimes Be Useful More Complex Types of Control Systems—Feed-Forwardand Adaptive Control PHYSIOLOGICAL VARIABILITY SUMMARY—AUTOMATICITY OF THE BODY Bibliography Chapter 2: The Cell and Its Functions ORGANIZATION OF THE CELL Water Ions Proteins Lipids Carbohydrates CELL STRUCTURE MEMBRANOUS STRUCTURES OF THE CELL Cell Membrane The Cell Membrane Lipid Barrier Impedes Penetrationby Water-Soluble Substances Integral and Peripheral Cell Membrane Proteins Membrane Carbohydrates—The Cell “Glycocalyx” CYTOPLASM AND ITS ORGANELLES Endoplasmic Reticulum Ribosomes and the Rough (Granular) Endoplasmic Reticulum Smooth (Agranular) Endoplasmic Reticulum Golgi Apparatus Lysosomes Peroxisomes Secretory Vesicles Mitochondria Cell Cytoskeleton—Filament and Tubular Structures Nucleus Nuclear Membrane Nucleoli and Formation of Ribosomes COMPARISON OF THE ANIMAL CELL WITH PRECELLULAR FORMS OF LIFE FUNCTIONAL SYSTEMS OF THE CELL ENDOCYTOSIS—INGESTION BY THE CELL Pinocytosis Phagocytosis LYSOSOMES DIGEST PINOCYTOTIC AND PHAGOCYTIC FOREIGN SUBSTANCES INSIDE THE CELL Lysosomes and Regression of Tissues and Autolysis of Damaged Cells Autophagy and Recycling of Cell Organelles SYNTHESIS OF CELLULAR STRUCTURES BY ENDOPLASMIC RETICULUM AND GOLGI APPARATUS Endoplasmic Reticulum Functions Proteins Synthesis by the Rough Endoplasmic Reticulum Lipid Synthesis by the Smooth Endoplasmic Reticulum Other Functions of the Endoplasmic Reticulum Golgi Apparatus Functions Synthetic Functions of the Golgi Apparatus Processing of Endoplasmic Secretions by the Golgi Apparatus—Formation of Vesicles Types of Vesicles Formed by the Golgi Apparatus—Secretory Vesicles and Lysosomes Use of Intracellular Vesicles to Replenish CellularMembranes THE MITOCHONDRIA EXTRACT ENERGY FROM NUTRIENTS Functional Characteristics of Adenosine Triphosphate Chemical Processes in the Formation of ATP—Role of the Mitochondria Uses of ATP for Cellular Function LOCOMOTION OF CELLS AMEBOID MOVEMENT Mechanism of Ameboid Locomotion Types of Cells That Exhibit Ameboid Locomotion Control of Ameboid Locomotion—Chemotaxis CILIA AND CILIARY MOVEMENTS Mechanism of Ciliary Movement Nonmotile Primary Cilia Serve as Cell Sensory “Antennae” Bibliography Chapter 3: Genetic Control of Protein Synthesis, Cell Function, and Cell Reproduction CELL NUCLEUS GENES CONTROL PROTEIN SYNTHESIS Building Blocks of DNA Nucleotides Nucleotides Are Organized to Form Two Strands of DNA Loosely Bound to Each Other GENETIC CODE TRANSCRIPTION—TRANSFER OF CELL NUCLEUS DNA CODE TO CYTOPLASM RNA CODE RNA IS SYNTHESIZED IN THE NUCLEUS FROM A DNA TEMPLATE Building Blocks of RNA Formation of RNA Nucleotides “Activation” of RNA Nucleotides RNA CHAIN ASSEMBLY FROM ACTIVATED NUCLEOTIDES USING THE DNA STRAND AS A TEMPLATE There Are Several Different Types of RNA MESSENGER RNA—THE CODONS RNA Codons for the Different Amino Acids TRANSFER RNA—THE ANTICODONS RIBOSOMAL RNA Formation of Ribosomes in the Nucleolus miRNA AND SMALL INTERFERING RNA TRANSLATION—FORMATION OF PROTEINS ON THE RIBOSOMES Polyribosomes Many Ribosomes Attach to the Endoplasmic Reticulum Chemical Steps in Protein Synthesis Peptide Linkage—Combination of Amino Acids SYNTHESIS OF OTHER SUBSTANCES IN THE CELL CONTROL OF GENE FUNCTION AND BIOCHEMICAL ACTIVITY IN CELLS GENETIC REGULATION The Promoter Controls Gene Expression Other Mechanisms for Control of Transcription by the Promoter CONTROL OF INTRACELLULAR FUNCTION BY ENZYME REGULATION Enzyme Inhibition Enzyme Activation Summary THE DNA–GENETIC SYSTEM CONTROLS CELL REPRODUCTION Life Cycle of the Cell Cell Reproduction Begins with Replication of DNA DNA Replication DNA Repair, DNA “Proofreading,” and “Mutation” CHROMOSOMES AND THEIR REPLICATION CELL MITOSIS Mitotic Apparatus: Function of the Centrioles Prophase Prometaphase Metaphase Anaphase Telophase CONTROL OF CELL GROWTH AND CELL REPRODUCTION Telomeres Prevent the Degradation of Chromosomes Regulation of Cell Size CELL DIFFERENTIATION APOPTOSIS—PROGRAMMED CELL DEATH CANCER Invasive Characteristic of the Cancer Cell Why Do Cancer Cells Kill? Bibliography Unit II: Membrane Physiology, Nerve, and Muscle Chapter 4: Transport of Substances Through Cell Membranes THE CELL MEMBRANE IS A LIPID BILAYER WITH CELL MEMBRANE TRANSPORT PROTEINS “Diffusion” Versus “Active Transport” DIFFUSION DIFFUSION THROUGH THE CELL MEMBRANE Diffusion of Lipid-Soluble Substances Through the Lipid Bilayer Diffusion of Water and Other Lipid-Insoluble Molecules Through Protein Channels DIFFUSION THROUGH PROTEIN PORES AND CHANNELS—SELECTIVE PERMEABILITY AND “GATING” OF CHANNELS Selective Permeability of Protein Channels Gating of Protein Channels Open-State Versus Closed-State of Gated Channels Patch Clamp Method for Recording Ion Current Flow Through Single Channels FACILITATED DIFFUSION REQUIRESMEMBRANE CARRIER PROTEINS FACTORS THAT AFFECT NET RATE OF DIFFUSION Net Diffusion Rate Is Proportional to the Concentration Difference Across a Membrane Membrane Electrical Potential and Diffusion ofIons—The “Nernst Potential” Effect of a Pressure Difference Across the Membrane OSMOSIS ACROSS SELECTIVELY PERMEABLE MEMBRANES—“NETDIFFUSION” OF WATER Osmotic Pressure Importance of Number of Osmotic Particles (Molar Concentration) in Determining Osmotic Pressure Osmolality—The Osmole Relationship of Osmolality to Osmotic Pressure The Term Osmolarity ACTIVE TRANSPORT OF SUBSTANCES THROUGH MEMBRANES Primary Active Transport and Secondary Active Transport PRIMARY ACTIVE TRANSPORT Sodium-Potassium Pump Transports Sodium Ions Out of Cells and Potassium Ions into Cells The Na+-K+ Pump Is Important for Controlling Cell Volume Electrogenic Nature of the Na+-K+ Pump Primary Active Transport of Calcium Ions Primary Active Transport of Hydrogen Ions Energetics of Primary Active Transport SECONDARY ACTIVE TRANSPORT—CO-TRANSPORT AND COUNTER-TRANSPORT Co-Transport of Glucose and Amino Acids Along with Sodium Ions Sodium Counter-Transport of Calcium and Hydrogen Ions ACTIVE TRANSPORT THROUGH CELLULAR SHEETS Bibliography Chapter 5: Membrane Potentials and Action Potentials Basic Physics of Membrane Potentials Membrane Potentials Caused by Ion Concentration Differences Across a Selectively Permeable Membrane The Nernst Equation Describes the Relationship of Diffusion Potential to the Ion Concentration Difference Across a Membrane The Goldman Equation Is Used to Calculate the Diffusion Potential When the Membrane Is Permeable to Several Different Ions Measuring the Membrane Potential Resting Membrane Potential of Neurons Active Transport of Sodium and Potassium Ions Through the Membrane—the Sodium-­Potassium (Na+-K+) Pump Leakage of Potassium Through the Nerve Cell Membrane Origin of the Normal Resting Membrane Potential Contribution of the Potassium Diffusion Potential Contribution of Sodium Diffusion Through the Nerve Membrane Contribution of the Na+­K+ Pump Neuron Action Potential Resting Stage Depolarization Stage Repolarization Stage Voltage­Gated Sodium and Potassium Channels Activation and Inactivation of the Voltage­Gated Sodium Channel Activation of the Sodium Channel Inactivation of the Sodium Channel Voltage-Gated Potassium Channel and Its Activation SUMMARY OF EVENTS THAT CAUSE THE ACTION POTENTIAL Initiation of the Action Potential A Positive­Feedback Cycle Opens the Sodium Channels Initiation of the Action Potential Occurs Only After the Threshold Potential is Reached Propagation of the Action Potential Direction of Propagation All-or-Nothing Principle RE-ESTABLISHING SODIUM AND POTASSIUM IONIC GRADIENTS AFTER ACTION POTENTIALS ARE COMPLETED—IMPORTANCE OF ENERGY METABOLISM Plateau in Some Action Potentials Rhythmicity of Some Excitable Tissues—Repetitive Discharge Re-Excitation Process Necessary for Spontaneous Rhythmicity Special Characteristics of Signal Transmission in Nerve Trunks Myelinated and Unmyelinated Nerve Fibers Saltatory Conduction in Myelinated Fibers from Node to Node Velocity of Conduction in Nerve Fibers Excitation—The Process of Eliciting the Action Potential Threshold for Excitation and Acute Local Potentials REFRACTORY PERIOD AFTER AN ACTION POTENTIAL, DURING WHICH A NEW STIMULUS CANNOT BE ELICITED Bibliography Chapter 6: Contraction of Skeletal Muscle PHYSIOLOGICAL ANATOMY OF SKELETAL MUSCLE The Sarcolemma Is a Thin Membrane Enclosing a Skeletal Muscle Fiber Myofibrils Are Composed of Actin and Myosin Filaments Titin Filamentous Molecules Keep the Myosin and Actin Filaments in Place Sarcoplasm Is the Intracellular Fluid Between Myofibrils Sarcoplasmic Reticulum Is a Specialized Endoplasmic Reticulum of Skeletal Muscle GENERAL MECHANISM OF MUSCLE CONTRACTION MOLECULAR MECHANISM OF MUSCLE CONTRACTION Muscle Contraction Occurs by a Sliding Filament Mechanism Molecular Characteristics of the Contractile Filaments Myosin Filaments Are Composed of Multiple Myosin Molecules Adenosine Triphosphatase Activity of the Myosin Head Actin Filaments Are Composed of Actin, Tropomyosin, and Troponin Tropomyosin Molecules Troponin and Its Role in Muscle Contraction Interaction of One Myosin Filament, Two Actin Filaments, and Calcium Ions to Cause Contraction Inhibition of the Actin Filament by the Troponin-Tropomyosin Complex Activation of the Actin Filament by Calcium Ions Interaction of the Activated Actin Filament and the Myosin Cross-Bridges—The Walk-Along Theory of Contraction ATP Is the Energy Source for Contraction—Chemical Events in the Motion of the Myosin Heads Amount of Actin and Myosin Filament Overlap Determines Tension Developed by the Contracting Muscle Effect of Muscle Length on Force of Contraction in the Whole Intact Muscle ENERGETICS OF MUSCLE CONTRACTION Work Output During Muscle Contraction Three Sources of Energy for Muscle Contraction CHARACTERISTICS OF WHOLE MUSCLE CONTRACTION Isometric Contractions Do Not Shorten Muscle, Whereas Isotonic Contractions Shorten Muscle at a Constant Tension Characteristics of Isometric Twitches Recorded from Different Muscles Fast Versus Slow Muscle Fibers Slow Fibers (Type 1, Red Muscle) Fast Fibers (Type II, White Muscle) MECHANICS OF SKELETAL MUSCLECONTRACTION Motor Unit—All the Muscle Fibers Innervated by a Single Nerve Fiber Muscle Contractions of Different Force—Force Summation Multiple Fiber Summation Frequency Summation and Tetanization Maximum Strength of Contraction Changes in Muscle Strength at the Onset of Contraction—the Staircase Effect (Treppe) Skeletal Muscle Tone Muscle Fatigue REMODELING OF MUSCLE TO MATCH FUNCTION Muscle Hypertrophy and Muscle Atrophy Adjustment of Muscle Length Hyperplasia of Muscle Fibers Muscle Denervation Causes Rapid Atrophy Bibliography Chapter 7: Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling Neuromuscular Junction and Transmission of Impulses from Nerve Endings to Skeletal Muscle Fibers PHYSIOLOGIC ANATOMY OF THE NEUROMUSCULAR JUNCTION—THE MOTOR END PLATE SECRETION OF ACETYLCHOLINE BY THE NERVE TERMINALS Acetylcholine Opens Ion Channels on Postsynaptic Membranes Destruction of the Released Acetylcholine by Acetylcholinesterase End Plate Potential and Excitation of the Skeletal Muscle Fiber Safety Factor for Transmission at the Neuromuscular Junction—Fatigue of the Junction Muscle Action Potential Action Potentials Spread to the Interior of the Muscle Fiber by Way of Transverse Tubules Excitation-Contraction Coupling Transverse Tubule–Sarcoplasmic Reticulum System Release of Calcium Ions by the Sarcoplasmic Reticulum Calcium Pump Removes Calcium Ions from the Myofibrillar Fluid After Contraction Occurs Excitatory Pulse of Calcium Ions Bibliography Chapter 8: Excitation and Contraction of Smooth Muscle Contraction of Smooth Muscle Types of Smooth Muscle Multi-Unit Smooth Muscle Unitary Smooth Muscle Contractile Mechanism in Smooth Muscle Chemical Basis for Smooth Muscle Contraction Physical Basis for Smooth Muscle Contraction Comparison of Smooth Muscle Contraction and Skeletal Muscle Contraction Slow Cycling of the Myosin Cross-Bridges Low Energy Requirement to Sustain Smooth Muscle Contraction Slowness of Onset of Contraction and Relaxation of the Total Smooth Muscle Tissue Maximum Force of Contraction Is Often Greater in Smooth Muscle Than in Skeletal Muscle Latch Mechanism Facilitates Prolonged Holding of Contractions of Smooth Muscle Stress-Relaxation of Smooth Muscle Regulation of Contraction by Calcium Ions Calcium Ions Combine with Calmodulin to Cause Activation of Myosin Kinase and Phosphorylation of the Myosin Head Source of Calcium Ions That Cause Contraction Role of the Smooth Muscle Sarcoplasmic Reticulum Smooth Muscle Contraction Is Dependent on Extracellular Calcium Ion Concentration A Calcium Pump Is Required to Cause Smooth Muscle Relaxation Myosin Phosphatase Is Important in Cessation of Contraction Possible Mechanism for Regulating the Latch Phenomenon Nervous and Hormonal Control of Smooth Muscle Contraction Neuromuscular Junctions of Smooth Muscle Physiologic Anatomy of Smooth Muscle Neuromuscular Junctions Excitatory and Inhibitory Transmitter Substances Secretedat the Smooth Muscle Neuromuscular Junction Membrane Potentials and Action Potentials in Smooth Muscle Membrane Potentials in Smooth Muscle Action Potentials in Unitary Smooth Muscle Spike Potentials Action Potentials with Plateaus Calcium Channels Are Important in Generating the Smooth Muscle Action Potential Slow Wave Potentials in Unitary Smooth Muscle Can Lead to Spontaneous Generation of Action Potentials Excitation of Visceral Smooth Muscle by Muscle Stretch DEPOLARIZATION OF MULTI-UNIT SMOOTH MUSCLE WITHOUT ACTION POTENTIALS Local Tissue Factors and Hormones Can Cause Smooth Muscle Contraction Without Action Potentials Smooth Muscle Contraction in Response to Local Tissue Chemical Factors Effects of Hormones on Smooth Muscle Contraction Mechanisms of Smooth Muscle Excitation or Inhibition by Hormones or Local Tissue Factors Bibliography Unit III: The Heart Chapter 9: Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves Physiology of Cardiac Muscle Cardiac Muscle Anatomy Left Ventricular Rotation (Twist) Aids Left Ventricular Ejection and Relaxation Cardiac Muscle Is a Syncytium ACTION POTENTIALS IN CARDIAC MUSCLE What Causes the Long Action Potential and Plateau in Cardiac Muscle Phases of Cardiac Muscle Action Potential Phase 0 (Depolarization): Fast Sodium Channels Open Phase 1 (Initial Repolarization): Fast Sodium Channels Close Phase 2 (Plateau): Calcium Channels Open and Fast Potassium Channels Close Phase 3 (Rapid Repolarization): Calcium Channels Close and Slow Potassium Channels Open Phase 4 (Resting Membrane Potential) Velocity of Signal Conduction in Cardiac Muscle Refractory Period of Cardiac Muscle EXCITATION-CONTRACTION COUPLING—FUNCTION OF CALCIUM IONS AND THE TRANSVERSE TUBULES Duration of Contraction Cardiac Cycle Diastole and Systole Increasing Heart Rate Decreases Duration of Cardiac Cycle Relationship of the Electrocardiogram to the Cardiac Cycle The Atria Function as Primer Pumps for the Ventricles FUNCTION OF THE VENTRICLES AS PUMPS The Ventricles Fill with Blood During Diastole Outflow of Blood from the Ventricles During Systole Period of Isovolumic (Isometric) Contraction Period of Ejection Period of Isovolumic (Isometric) Relaxation End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output THE HEART VALVES PREVENT BACKFLOW OF BLOOD DURING SYSTOLE Atrioventricular Valves Function of the Papillary Muscles Aortic and Pulmonary Artery Valves AORTIC PRESSURE CURVE GRAPHIC ANALYSIS OF VENTRICULAR PUMPING Volume-Pressure Diagram During the Cardiac Cycle; Cardiac Work Output Phase I: Period of Filling Phase II: Period of Isovolumic Contraction Phase III: Period of Ejection Phase IV: Period of Isovolumic Relaxation Concepts of Preload and Afterload Regulation of Heart Pumping INTRINSIC REGULATION OF HEART PUMPING—THE FRANK-STARLING MECHANISM What Is the Explanation of the Frank Starling Mechanism? Ventricular Function Curves Control of the Heart by the Sympathetic and Parasympathetic Nerves Mechanisms of Excitation of the Heart by the Sympathetic Nerves Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction Effect of Sympathetic or Parasympathetic Stimulationon the Cardiac Function Curve EFFECT OF POTASSIUM AND CALCIUMIONS ON HEART FUNCTION Effect of Potassium Ions Effect of Calcium Ions EFFECT OF TEMPERATURE ON HEART FUNCTION INCREASING THE ARTERIAL PRESSURE LOAD (UP TO A LIMIT) DOES NOT DECREASE CARDIAC OUTPUT Bibliography Chapter 10: Rhythmical Excitation of the Heart Specialized Excitatory and Conductive System of the Heart Sinus (Sinoatrial) Node AUTOMATIC ELECTRICAL RHYTHMICITYOF THE SINUS FIBERS Mechanism of Sinus Nodal Rhythmicity Leakiness of Sinus Nodal Fibers to Sodium and Calcium Causes Self-Excitation INTERNODAL AND INTERATRIAL PATHWAYS TRANSMIT CARDIAC IMPULSES THROUGH THE ATRIA THE ATRIOVENTRICULAR NODE DELAYS IMPULSE CONDUCTION FROM THE ATRIA TO THE VENTRICLES Cause of the Slow Conduction RAPID TRANSMISSION OF THE CARDIAC IMPULSE IN THE VENTRICULAR PURKINJE SYSTEM The A-V Bundle Is Normally a One-Way Conduction Path Distribution of the Purkinje Fibers in the Ventricles—Left and Right Bundle Branches TRANSMISSION OF THE CARDIAC IMPULSE IN THE VENTRICULAR MUSCLE SUMMARY OF THE SPREAD OF THE CARDIAC IMPULSE THROUGH THE HEART CONTROL OF EXCITATION ANDCONDUCTIONIN THE HEART The Sinus Node is the Normal Pacemaker of the Heart Abnormal Pacemakers—Ectopic Pacemaker ROLE OF THE PURKINJE SYSTEM IN CAUSING SYNCHRONOUS CONTRACTION OF THE VENTRICULAR MUSCLE SYMPATHETIC AND PARASYMPATHETIC NERVES CONTROL HEART RHYTHMICITY AND IMPULSE CONDUCTION BY THE CARDIAC NERVES Parasympathetic (Vagal) Stimulation Slows the Cardiac Rhythm and Conduction Mechanism of the Vagal Effects Sympathetic Stimulation Increases the Cardiac Rhythm and Conduction Mechanism of the Sympathetic Effect Bibliography Chapter 11: Fundamentals of Electrocardiography Waveforms of the Normal Electrocardiogram CARDIAC DEPOLARIZATION WAVES VERSUS REPOLARIZATION WAVES Relation of the Monophasic Action Potential of Ventricular Muscle to the QRS and T Waves in the Standard Electrocardiogram RELATIONSHIP OF ATRIAL AND VENTRICULAR CONTRACTION TO THE WAVES OF THE ELECTROCARDIOGRAM ELECTROCARDIOGRAPHIC CALIBRATION AND DISPLAY Normal Voltages in the Electrocardiogram P-Q or P-R Interval Q-T Interval Heart Rate as Determined from the Electrocardiogram FLOW OF CURRENT AROUND THE HEART DURING THE CARDIAC CYCLE Recording Electrical Potentials from a Partially Depolarized Mass of Syncytial Cardiac Muscle Flow of Electrical Currents in the Chest Around the Heart Electrocardiographic Leads Three Standard Bipolar Limb Leads Lead I Lead II Lead III Einthoven’s Triangle Einthoven’s Law Normal Electrocardiograms Recorded from the Three Standard Bipolar Limb Leads Precordial Leads Augmented Limb Leads Bibliography Chapter 12: Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities: Vectorial Analysis VECTORIAL ANALYSIS OF ELECTROCARDIOGRAMS VECTORS CAN REPRESENT ELECTRICAL POTENTIALS Resultant Vector in the Heart at Any Given Instant THE DIRECTION OF A VECTOR IS DENOTED IN TERMS OF DEGREES AXIS FOR EACH STANDARD BIPOLAR LEAD AND EACH UNIPOLAR LIMB LEAD VECTORIAL ANALYSIS OF POTENTIALS RECORDED IN DIFFERENT LEADS Vectorial Analysis of Potentials in the Three Standard Bipolar Limb Leads VECTORIAL ANALYSIS OF THE NORMAL ELECTROCARDIOGRAM VECTORS THAT OCCUR AT SUCCESSIVE INTERVALS DURING DEPOLARIZATION OF THE VENTRICLES—THE QRS COMPLEX ELECTROCARDIOGRAM DURING VENTRICULAR REPOLARIZATION—THE T WAVE ATRIAL DEPOLARIZATION—THE P WAVE Repolarization of the Atria—the Atrial T Wave MEAN ELECTRICAL AXIS OFTHE VENTRICULAR QRS AND ITS SIGNIFICANCE DETERMINING THE ELECTRICAL AXIS FROM STANDARD LEAD ELECTRO CARDIOGRAMS ABNORMAL VENTRICULAR CONDITIONS THAT CAUSE AXIS DEVIATION Change in the Position of the Heart in the Chest Hypertrophy of One Ventricle Vectorial Analysis of Left Axis Deviation Resulting from Hypertrophy of the Left Ventricle Vectorial Analysis of Right Axis Deviation Resulting from Hypertrophy of the Right Ventricle Bundle Branch Block Causes Axis Deviation Vectorial Analysis of Left Axis Deviation in Left Bundle Branch Block Vectorial Analysis of Right Axis Deviation in Right Bundle Branch Block CONDITIONS THAT CAUSE ABNORMAL VOLTAGES OF THE QRS COMPLEX INCREASED VOLTAGE IN THE STANDARD BIPOLAR LIMB LEADS DECREASED VOLTAGE OF THE ELECTROCARDIOGRAM Decreased Voltage Caused by Cardiac Myopathies Decreased Voltage Caused by Conditions Surrounding the Heart PROLONGED AND BIZARRE PATTERNS OF THE QRS COMPLEX CARDIAC HYPERTROPHY OR DILATION PROLONG THE QRS COMPLEX PURKINJE SYSTEM BLOCK PROLONGS THE QRS COMPLEX CONDITIONS THAT CAUSE BIZARRE QRS COMPLEXES CURRENT OF INJURY EFFECT OF CURRENT OF INJURY ON THE QRS COMPLEX THE J POINT IS THE ZERO REFERENCE POTENTIAL FOR ANALYZING CURRENT OF INJURY Use of the J Point in Plotting Axis of Injury Potential CORONARY ISCHEMIA AS A CAUSE OF INJURY POTENTIAL Acute Anterior Wall Infarction Posterior Wall Infarction Infarction in Other Parts of the Heart ECG Progression During and After Acute Coronary Thrombosis Q Waves on an ECG Represent Old Myocardial Infarction Current of Injury in Angina Pectoris ABNORMALITIES IN THE T WAVE EFFECT OF SLOW CONDUCTION OF THE DEPOLARIZATION WAVE ON THE CHARACTERISTICS OF THE T WAVE SHORTENED DEPOLARIZATION IN PORTIONS OF THE VENTRICULAR MUSCLE CAN CAUSE T-WAVE ABNORMALITIES Effect of Digitalis on the T Wave Bibliography Chapter 13: Cardiac Arrhythmias and Their Electrocardiographic Interpretation Abnormal Sinus Rhythms Tachycardia Bradycardia Bradycardia in Athletes Vagal Stimulation Causes Bradycardia Sinus Arrhythmia Heart Block Within the Intracardiac Conduction Pathways Sinoatrial Block Atrioventricular Block Incomplete Atrioventricular Block First-Degree Block—Prolonged P-R Interval Second-Degree Block Complete A-V Block (Third-Degree Block) Stokes-Adams Syndrome—Ventricular Escape INCOMPLETE INTRAVENTRICULAR BLOCK—ELECTRICAL ALTERNANS Premature Contractions Causes of Premature Contractions Premature Atrial Contractions Pulse Deficit A-V NODAL OR A-V BUNDLE PREMATURE CONTRACTIONS PREMATURE VENTRICULAR CONTRACTIONS Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction Disorders of Cardiac Repolarization—the Long QT Syndromes Paroxysmal Tachycardia Paroxysmal Atrial Tachycardia A-V Nodal Paroxysmal Tachycardia Ventricular Tachycardia Ventricular Fibrillation PHENOMENON OF RE-ENTRY—CIRCUS MOVEMENTS AS THE BASIS FOR VENTRICULAR FIBRILLATION CHAIN REACTION MECHANISM OF FIBRILLATION Fibrillation Caused by 60-Cycle Alternating Current ELECTROCARDIOGRAM IN VENTRICULAR FIBRILLATION VENTRICULAR DEFIBRILLATION HAND PUMPING OF THE HEART (CARDIOPULMONARY RESUSCITATION) AS AN AID TO DEFIBRILLATION Atrial Fibrillation Impaired Pumping of the Atria During Atrial Fibrillation ELECTROCARDIOGRAM IN ATRIAL FIBRILLATION IRREGULARITY OF VENTRICULAR RHYTHM DURING ATRIAL FIBRILLATION ELECTROSHOCK TREATMENT OF ATRIAL FIBRILLATION Atrial Flutter Cardiac Arrest Bibliography Unit IV: The Circulation Chapter 14: Overview of the Circulation: Pressure, Flow, and Resistance Physical Characteristics of the Circulation Functional Parts of the Circulation Volumes of Blood in the Different Parts of the Circulation Cross-Sectional Areas and Velocities of Blood Flow Pressures in the Various Portions of the Circulation Basic Principles of Circulatory Function Interrelationships of Pressure, Flow, and Resistance Blood Flow Laminar Flow of Blood in Vessels Parabolic Velocity Profile During Laminar Flow Turbulent Flow of Blood Under Some Conditions Blood Pressure Standard Units of Pressure Resistance to Blood Flow Units of Resistance Expression of Resistance in CGS Units Total Peripheral Vascular Resistance and Total Pulmonary Vascular Resistance Conductance of Blood in a Vessel Is the Reciprocal of Resistance Small Changes in Vessel Diameter Markedly Change Its Conductance Poiseuille’s Law Importance of the Vessel Diameter Fourth Power Law in Determining Arteriolar Resistance Resistance to Blood Flow in Series and Parallel Vascular Circuits Effect of Blood Hematocrit and Blood Viscosity on Vascular Resistance and Blood Flow Hematocrit—the Proportion of Blood That Is Red Blood Cells Increasing Hematocrit Markedly Increases Blood Viscosity Effects of Pressure on Vascular Resistance and Tissue Blood Flow Autoregulation Attenuates the Effect of Arterial Pressure on Tissue Blood Flow Pressure-Flow Relationship in Passive Vascular Beds Vascular Wall Tension Vascular Shear Stress Bibliography Chapter 15: Vascular Distensibility and Functions of the Arterial and Venous Systems Vascular Distensibility Units of Vascular Distensibility The Veins Are Much More Distensible Than the Arteries VASCULAR COMPLIANCE (OR VASCULAR CAPACITANCE) VOLUME-PRESSURE CURVES OF THE ARTERIAL AND VENOUS CIRCULATIONS Effect of Sympathetic Stimulation or Sympathetic Inhibition on the Volume-Pressure Relationships of the Arterial and Venous Systems Delayed Compliance (Stress-Relaxation) of Vessels Arterial Pressure Pulsations Abnormal Pressure Pulse Contours TRANSMISSION OF PRESSURE PULSES TO THE PERIPHERAL ARTERIES Pressure Pulses Are Damped in the Smaller Arteries, Arterioles, and Capillaries CLINICAL METHODS FOR MEASURINGSYSTOLIC AND DIASTOLIC PRESSURES Auscultatory Method Automated Oscillometric Method Normal Arterial Pressures as Measured by the Auscultatory and Oscillatory Methods Mean Arterial Pressure Veins and Their Functions VENOUS PRESSURES—RIGHT ATRIAL PRESSURE (CENTRAL VENOUS PRESSURE) AND PERIPHERAL VENOUS PRESSURES Venous Resistance and Peripheral Venous Pressure Effect of High Right Atrial Pressure on Peripheral Venous Pressure Effect of Intra-abdominal Pressure on Venous Pressures of the Leg Effect of Gravitational Pressure on Venous Pressure Effect of the Gravitational Factor on Arterial and Other Pressures Venous Valves and the Venous Pump: Their Effects on Venous Pressure Venous Valve Incompetence Causes Varicose Veins BLOOD RESERVOIR FUNCTION OF THE VEINS SPECIFIC BLOOD RESERVOIRS THE SPLEEN IS A RESERVOIR FOR RED BLOOD CELLS Bibliography Chapter 16: The Microcirculation and Lymphatic System: Capillary Fluid Exchange, Interstitial Fluid, and Lymph Flow Structure of the Microcirculation and Capillary System Structure of the Capillary Wall Pores in the Capillary Membrane Special Types of Pores in Capillaries of Certain Organs Flow of Blood in the Capillaries—Vasomotion Regulation of Vasomotion Average Function of the Capillary System EXCHANGE OF WATER, NUTRIENTS, AND OTHER SUBSTANCES BETWEEN THE BLOOD AND INTERSTITIAL FLUID Diffusion Through the Capillary Membrane Is the Most Important Means of Transferring Substances Between Plasma and Interstitial Fluid Lipid-Soluble Substances Diffuse Directly Through the Cell Membranes of the Capillary Endothelium Water-Soluble, Non–Lipid-Soluble Substances Diffuse Through Intercellular Pores in the Capillary Membrane Effect of Molecular Size on Passage Through the Pores Diffusion Through the Capillary Membrane Is Proportional to the Concentration Difference Between the Two Sides of the Membrane Interstitium and Interstitial Fluid Gel in the Interstitium Free Fluid in the Interstitium Fluid Filtration Across Capillaries Hydrostatic and Colloid Osmotic Forces Determine Fluid Movement Through the Capillary Membrane Capillary Hydrostatic Pressure INTERSTITIAL FLUID HYDROSTATIC PRESSURE Interstitial Fluid Pressures in Tightly Encased Tissues Summary: Interstitial Fluid Pressure in Loose Subcutaneous Tissue Usually Subatmospheric Pumping by the Lymphatic System—Basic Cause of the Negative Interstitial Fluid Pressure Plasma Colloid Osmotic Pressure Plasma Proteins Cause Colloid Osmotic Pressure Normal Values for Plasma Colloid Osmotic Pressure INTERSTITIAL FLUID COLLOID OSMOTIC PRESSURE FLUID VOLUME EXCHANGE THROUGH THE CAPILLARY MEMBRANE Analysis of the Forces Causing Filtration at the Arterial End of the Capillary Analysis of Reabsorption at the Venous End of the Capillary STARLING EQUILIBRIUM FOR CAPILLARY EXCHANGE CAPILLARY FILTRATION COEFFICIENT Effect of Abnormal Imbalance of Forces at the Capillary Membrane Lymphatic System Lymph Channels of the Body Terminal Lymphatic Capillaries and Their Permeability Formation of Lymph Rate of Lymph Flow Effect of Interstitial Fluid Pressure on Lymph Flow Lymphatic Pump Increases Lymph Flow. Valves exist in all lymph channels. Figure 16-­9 shows typical valves for collecting lympha... Pumping Caused by External Intermittent Compression of the Lymphatics. In addition to the pumping caused by intrinsic intermitte... Lymphatic Capillary Pump. The terminal lymphatic capillary is also capable of pumping lymph, in addition to the pumping by the l... Summary of Factors That Determine Lymph Flow. From the previous discussion, one can see that the two primary factors that determ... Lymphatic System Plays a Key Role in Controlling Interstitial Fluid Protein Concentration, Volume, and Pressure Significance of Negative Interstitial Fluid Pressure for Holding Body Tissues Together Bibliography Chapter 17: Local and Humoral Control of Tissue Blood Flow Local Control of Blood Flow in Response to Tissue Needs Variations in Blood Flow in Different Tissues and Organs Importance of Blood Flow Control by the Local Tissues Mechanisms of Blood Flow Control Acute Control of Local Blood Flow Increases in Tissue Metabolism Increase Tissue Blood Flow Reduced Oxygen Availability Increases Tissue Blood Flow Vasodilator Theory for Acute Local Blood Flow Regulation—Possible Special Role of Adenosine Oxygen Demand Theory for Local Blood Flow Control Possible Role of Other Nutrients Besides Oxygen in Control of Local Blood Flow Special Examples of Acute Metabolic Control of Local Blood Flow Reactive Hyperemia Occurs After Tissue Blood Supply Is Blocked for a Short Time Active Hyperemia Occurs When Tissue Metabolic Rate Increases Autoregulation of Blood Flow During Changes in Arterial Pressure—Metabolic and Myogenic Mechanisms Special Mechanisms for Acute Blood Flow Control in Specific Tissues Control of Tissue Blood Flow: Endothelium Derived Relaxing or Constricting Factors Nitric Oxide Is a Vasodilator Released from Healthy Endothelial Cells Endothelin Is a Powerful Vasoconstrictor Released From Damaged Endothelium Long Term Blood Flow Regulation Blood Flow Regulation by Changes in Tissue Vascularity Role of Oxygen in Long-Term Regulation Importance of Vascular Growth Factors in Formation of New Blood Vessels Vascularity Determined by Maximum Blood Flow Need, Not by Average Need Blood Flow Regulation by Development of Collateral Circulation Vascular Remodeling in Response to Chronic Changes in Blood Flow or Blood Pressure Humoral Control of the Circulation Vasoconstrictors Norepinephrine and Epinephrine Angiotensin II Vasopressin Vasodilators Bradykinin Histamine Most Vasodilators or Vasoconstrictors Have Little Effecton Long-Term Blood Flow Unless They Alter the Metabolic Rate of the Tissues Bibliography Chapter 18: Nervous Regulation of the Circulation and Rapid Control of Arterial Pressure Nervous Regulation of the Circulation Autonomic Nervous System Sympathetic Nervous System Sympathetic Innervation of the Blood Vessels Sympathetic Stimulation Increases Heart Rate and Contractility Parasympathetic Stimulation Decreases Heart Rate and Contractility Sympathetic Vasoconstrictor System and Its Control by the Central Nervous System Vasomotor Center in the Brain and Its Control of the Vasoconstrictor System Continuous Partial Constriction of Blood Vessels by Sympathetic Vasoconstrictor Tone Control of Heart Activity by the Vasomotor Center Control of the Vasomotor Center by Higher Nervous Centers Norepinephrine Is the Sympathetic Vasoconstrictor Neurotransmitter Adrenal Medullae and Their Relationship to the Sympathetic Vasoconstrictor System Role of the Nervous System in Rapid Control of Arterial Pressure Nervous Control of Arterial Pressure Is Rapid INCREASES IN ARTERIAL PRESSURE DURING MUSCLE EXERCISE AND OTHER STRESSES Reflex Mechanisms for Maintaining Normal Arterial Pressure Baroreceptor Arterial Pressure Control System—Baroreceptor Reflexes Physiologic Anatomy of the Baroreceptors and Their Innervation Response of the Baroreceptors to Changes in Arterial Pressure Circulatory Reflex Initiated by the Baroreceptors Baroreceptors Attenuate Blood Pressure Changes During Changes in Body Posture Pressure Buffer Function of the Baroreceptor Control System Are the Baroreceptors Important in Long-Term Regulation of Arterial Pressure? Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors—Effect of Low Oxygen on Arterial Pressure Atrial and Pulmonary Artery Reflexes Regulate Arterial Pressure Atrial Reflexes That Activate the Kidneys—The Volume Reflex Increased Atrial Pressure Raises Heart Rate—Bainbridge Reflex DECREASED BLOOD FLOW TO BRAIN VASOMOTOR CENTER ELICITS INCREASED BLOOD PRESSURE—CNS ISCHEMIC RESPONSE Importance of CNS Ischemic Response as a Regulator of Arterial Pressure Cushing Reaction to Increased Pressure Around the Brain SPECIAL FEATURES OF NERVOUS CONTROL OF ARTERIAL PRESSURE ROLE OF THE SKELETAL NERVES AND SKELETAL MUSCLES IN INCREASING CARDIAC OUTPUT AND ARTERIAL PRESSURE Abdominal Compression Reflex Increases Cardiac Output and Arterial Pressure Skeletal Muscle Contraction Increases Cardiac Output and Arterial Pressure During Exercise RESPIRATORY WAVES IN THE ARTERIAL PRESSURE Arterial Pressure Vasomotor Waves—Oscillation of Pressure Reflex Control Systems Oscillation of Baroreceptor and Chemoreceptor Reflexes Oscillation of CNS Ischemic Response Bibliography Chapter 19: Role of the Kidneys in Long-Term Control of Arterial Pressure and in Hypertension: The Integrated System for Arterial Pressure Regulation Renal–Body Fluid System for Arterial Pressure Control QUANTITATION OF PRESSURE DIURESIS AS A BASIS FOR ARTERIAL PRESSURE CONTROL Experiment Demonstrating the Renal–Body Fluid System for Arterial Pressure Control Renal–Body Fluid Mechanism Provides Nearly Infinite Feedback Gain for Long-term Arterial Pressure Control Two Key Determinants of Long-Term Arterial Pressure Chronic Renal Output Curve Much Steeper Than the Acute Curve Failure of Increased Total Peripheral Resistance to Elevate Long-Term Level of Arterial Pressure if Fluid Intake and Renal Function Do Not Change Increased Fluid Volume Can Elevate Arterial Pressure by Increasing Cardiac Output or Total Peripheral Resistance Importance of Salt (NaCl) in the Renal–Body Fluid Schema for Arterial Pressure Regulation CHRONIC HYPERTENSION (HIGH BLOOD PRESSURE) CAUSED BY IMPAIRED RENAL FUNCTION Experimental Volume-Loading Hypertension Caused by Reduced Kidney Mass and Increased Salt Intake Sequential Changes in Circulatory Function During Development of Volume-Loading Hypertension Volume-Loading Hypertension in Patients Who Have No Kidneys but Are Being Maintained With an Artificial Kidney Hypertension Caused by Excess Aldosterone Role of the Renin­Angiotensin System in Arterial Pressure Control COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM Rapidity and Intensity of the Vasoconstrictor Pressure Response to the Renin-­Angiotensin System Angiotensin II Causes Renal Retention of Salt and Water—An Important Means for Long­Term Control of Arterial Pressure Mechanisms of the Direct Renal Effects of Angiotensin II to Cause Renal Retention of Salt and Water Angiotensin II Increases Kidney Salt and Water Retention by Stimulating Aldosterone Role of the Renin­Angiotensin System in Maintaining a Normal Arterial Pressure Despite Large Variations in Salt Intake HYPERTENSION CAUSED BY RENIN-SECRETING TUMOR OR RENAL ISCHEMIA One­Kidney Goldblatt Hypertension Two­Kidney Goldblatt Hypertension Hypertension Caused by Diseased Kidneys That Secrete Renin Chronically Primary (Essential) Hypertension Graphic Analysis of Arterial Pressure Control in Essential Hypertension Treatment of Essential Hypertension Summary of Integrated Multifaceted Systems for Arterial Pressure Regulation Arterial Pressure Control Mechanisms That Act Within Seconds or Minutes Arterial Pressure Control Mechanisms That Act After Many Minutes Long­Term Mechanisms for Arterial Pressure Regulation Bibliography Chapter 20: Cardiac Output, Venous Return, and Their Regulation Normal Values for Cardiac Output at Rest and During Activity Effect of Age on Cardiac Output Control of Cardiac Output by Venous Return—Frank-Starling Mechanism of the Heart Cardiac Output Is the Sum of All Tissue Blood Flows—Tissue Metabolism Regulates Most Local Blood Flow Cardiac Output Varies Inversely With Total Peripheral Resistance When Arterial Pressure Is Unchanged Limits for the Cardiac Output Factors That Cause a Hypereffective Heart Nervous Excitation Can Increase Heart Pumping Heart Hypertrophy Can Increase Pumping Effectiveness Factors That Cause a Hypoeffective Heart Nervous System Regulation of Cardiac Output Importance of Nervous System For Maintaining Arterial Pressure When Peripheral Blood Vessels Are Dilated and Venous Return and Cardiac Output Increase Effect of Nervous System to Increase Arterial Pressure During Exercise CARDIAC OUTPUT CURVES USED IN QUANTITATIVE ANALYSIS OF CARDIAC OUTPUT REGULATION Effect of External Pressure Outside the Heart on Cardiac Output Curves Combinations of Different Patterns of Cardiac Output Curves VENOUS RETURN CURVES Normal Venous Return Curve Plateau in Venous Return Curve at Negative Atrial Pressures Caused by Collapse of the Large Veins Mean Circulatory Filling Pressure, Mean Systemic Filling Pressure—Effects on Venous Return Increased Blood Volume Raises Mean Circulatory Filling Pressure Sympathetic Nervous Stimulation Increases Mean Circulatory Filling Pressure Mean Systemic Filling Pressure and Relationship to Mean Circulatory Filling Pressure Effect on Venous Return Curve of Changes in Mean Systemic Filling Pressure When Pressure Gradient for Venous Return Is Zero There Is No Venous Return Resistance to Venous Return Effect of Resistance to Venous Return on the Venous Return Curve Combinations of Venous Return Curve Patterns ANALYSIS OF CARDIAC OUTPUT AND RIGHT ATRIAL PRESSURE BY SIMULTANEOUS CARDIAC OUTPUT AND VENOUS RETURN CURVES Effect of Increased Blood Volume on Cardiac Output Compensatory Effects Initiated in Response to Increased Blood Volume Effect of Sympathetic Stimulation on Cardiac Output Effect of Sympathetic Inhibition on Cardiac Output Effect of Opening a Large Arteriovenous Fistula Other Analyses of Cardiac Output Regulation Methods For Measuring Cardiac Output Pulsatile Output of the Heart Measured by Electromagnetic or Ultrasonic Flowmeter Measurement of Cardiac Output Using the Oxygen Fick Principle Indicator Dilution Method Echocardiography Thoracic Electrical Bioimpedance Method Bibliography Chapter 21: Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and Ischemic Heart Disease Blood Flow Regulation in Skeletal Muscle at Rest and During Exercise Skeletal Muscle Blood Flow Rate Blood Flow During Muscle Contractions Increased Blood Flow in Muscle Capillaries During Exercise. During rest, some muscle capillaries have little or no flowing blood... Control of Skeletal Muscle Blood Flow Decreased Oxygen in Muscle Greatly Enhances Flow Nervous Control of Muscle Blood Flow CIRCULATORY READJUSTMENTS DURING EXERCISE Effects of Sympathetic Activation Sympathetic Stimulation May Increase Arterial Pressure During Exercise Why Is Increased Arterial Pressure During Exercise Important? Importance of Increased Cardiac Output During Exercise Graphic Analysis of Changes in Cardiac Output During Heavy Exercise Coronary Circulation PHYSIOLOGIC ANATOMY OF THE CORONARY BLOOD SUPPLY NORMAL CORONARY BLOOD FLOWAVERAGES 5% OF CARDIAC OUTPUT Cardiac Muscle Compression Causes Phasic Changes in Coronary Blood Flow During Systole and Diastole Epicardial Versus Subendocardial Coronary Blood Flow—Effect of Intramyocardial Pressure CONTROL OF CORONARY BLOOD FLOW Local Muscle Metabolism Is the Primary Controller of Coronary Flow Oxygen Demand Is a Major Factor in Local Coronary Blood Flow Regulation Nervous Control of Coronary Blood Flow Direct Effects of Nervous Stimuli on Coronary Vasculature SPECIAL FEATURES OF CARDIAC MUSCLE METABOLISM ISCHEMIC HEART DISEASE Atherosclerosis Is a Major Cause of Ischemic Heart Disease Acute Coronary Artery Occlusion Lifesaving Value of Collateral Circulation in the Heart Myocardial Infarction Subendocardial Infarction CAUSES OF DEATH AFTER ACUTE CORONARY OCCLUSION Decreased Cardiac Output—Systolic Stretch and Cardiac Shock Damming of Blood in the Body’s Venous System Fibrillation of the Ventricles After Myocardial Infarction Rupture of Infarcted Area STAGES OF RECOVERY FROM ACUTE MYOCARDIAL INFARCTION Replacement of Dead Muscle by Scar Tissue Value of Rest in Treating Myocardial Infarction HEART FUNCTION AFTER RECOVERY FROM MYOCARDIAL INFARCTION PAIN IN CORONARY HEART DISEASE Angina Pectoris (Cardiac Pain) Drug Treatment SURGICAL TREATMENT OF CORONARYARTERY DISEASE Aortic-Coronary Bypass Surgery Coronary Angioplasty Bibliography Chapter 22: Cardiac Failure CIRCULATORY DYNAMICS IN CARDIAC FAILURE ACUTE EFFECTS OF MODERATE CARDIAC FAILURE Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes CHRONIC STAGE OF FAILURE—FLUID RETENTION AND COMPENSATED CARDIAC OUTPUT Renal Retention of Fluid and Increase inBlood Volume Occur for Hours to Days Moderate Fluid Retention in Cardiac Failure Can Be Beneficial Detrimental Effects of Excess Fluid Retention in Severe Cardiac Failure Recovery of the Heart After Myocardial Infarction Cardiac Output Curve After Partial Recovery SUMMARY OF CHANGES AFTER ACUTE CARDIAC FAILURE—COMPENSATED HEART FAILURE Compensated Heart Failure DYNAMICS OF SEVERE CARDIAC FAILURE—DECOMPENSATED HEART FAILURE Graphic Analysis of Decompensated Heart Failure Treatment of Decompensation Mechanism of Action of Cardiotonic Drugs UNILATERAL LEFT HEART FAILURE LOW-OUTPUT CARDIAC FAILURE—CARDIOGENIC SHOCK Vicious Cycle of Cardiac Deterioration in Cardiogenic Shock Physiology of Cardiogenic Shock Treatment EDEMA IN PATIENTS WITH CARDIAC FAILURE Acute Cardiac Failure Does Not Cause Immediate Peripheral Edema LONG-TERM FLUID RETENTION BY THE KIDNEYS CAUSES PERIPHERAL EDEMA IN PERSISTING HEART FAILURE Role of Natriuretic Peptides in Delaying Onset of Cardiac Decompensation Acute Pulmonary Edema in Late-Stage Heart Failure—Another Lethal Vicious Cycle CARDIAC RESERVE Diagnosis of Low Cardiac Reserve—Exercise Test QUANTITATIVE GRAPHIC ANALYSIS OF CARDIAC FAILURE Graphic Analysis of Acute Heart Failure and Chronic Compensation Acute Heart Attack Reduces Cardiac Output Curve Sympathetic Reflexes Raise Cardiac Output and Venous Return Curves Compensation During the Next Few Days Further Increases Cardiac Output and Venous Return Curves Graphic Analysis of Decompensated Cardiac Failure Treatment of Decompensated Heart Disease With Digitalis HEART FAILURE WITH DIASTOLIC DYSFUNCTION AND NORMAL EJECTION FRACTION HIGH-OUTPUT CARDIAC FAILURE Arteriovenous Fistula Increases Venous Return Beriberi Weakens the Heart, Causes Fluid Retention by the Kidneys, and Increases Venous Return Bibliography Chapter 23: Heart Valves and Heart Sounds; Valvular and Congenital Heart Defects HEART SOUNDS NORMAL HEART SOUNDS The First Heart Sound Is Associated With Closure of A-V The Second Heart Sound Is Associated With Closure of the Aortic and Pulmonary Valves Duration and Pitch of First and Second Heart Sounds The Third Heart Sound Occurs at the Beginning of the Middle Third of Diastole Atrial Contraction—Fourth Heart Sound Chest Surface Areas for Auscultation of Normal Heart Sounds Phonocardiogram VALVULAR LESIONS Rheumatic Valvular Lesions Aging and Aortic Valve Stenosis Heart Murmurs Caused by Valvular Lesions Systolic Murmur of Aortic Stenosis Diastolic Murmur of Aortic Regurgitation Systolic Murmur of Mitral Regurgitation Diastolic Murmur of Mitral Stenosis Phonocardiograms of Valvular Murmurs ABNORMAL CIRCULATORY DYNAMICS IN VALVULAR HEART DISEASE CIRCULATORY DYNAMICS IN AORTIC STENOSIS AND AORTIC REGURGITATION Hypertrophy of Left Ventricle Increase in Blood Volume Aortic Valvular Lesions May Be Associated With Inadequate Coronary Blood Flow Eventual Failure of Left Ventricle and Development of Pulmonary Edema DYNAMICS OF MITRAL STENOSIS AND MITRAL REGURGITATION Pulmonary Edema in Mitral Valvular Disease Enlarged Left Atrium and Atrial Fibrillation Compensation in Early Mitral Valvular Disease CIRCULATORY DYNAMICS DURING EXERCISE IN PATIENTS WITH VALVULAR LESIONS ABNORMAL CIRCULATORY DYNAMICS IN CONGENITAL HEART DEFECTS PATENT DUCTUS ARTERIOSUS—A LEFT-TO-RIGHT SHUNT Closure of Ductus Arteriosus After Birth Dynamics of the Circulation With a Persistent Patent Ductus Recirculation Through the Lungs Diminished Cardiac and Respiratory Reserve Heart Sounds: Machinery Murmur Surgical Treatment TETRALOGY OF FALLOT—A RIGHT-TO-LEFT SHUNT Abnormal Circulatory Dynamics Surgical Treatment CAUSES OF CONGENITAL ANOMALIES USE OF EXTRACORPOREAL CIRCULATION DURING CARDIAC SURGERY HYPERTROPHY OF THE HEART IN VALVULAR AND CONGENITAL HEART DISEASE Detrimental Effects of Late Stages of Cardiac Hypertrophy Bibliography Chapter 24: Circulatory Shock and Its Treatment Physiological Causes of Shock Circulatory Shock Caused by Decreased Cardiac Output CIRCULATORY SHOCK WITHOUT DIMINISHED CARDIAC OUTPUT WHAT HAPPENS TO THE ARTERIAL PRESSURE IN CIRCULATORY SHOCK? TISSUE DETERIORATION IS THE END RESULT OF CIRCULATORY SHOCK Stages of Shock Shock Caused by Hypovolemia—Hemorrhagic Shock Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure Sympathetic Reflex Compensations in Shock—Their Special Value to Maintain Arterial Pressure Greater Effect of Sympathetic Nervous Reflexes in Maintaining Arterial Pressure Than in Maintaining Cardiac Output Protection of Coronary and Cerebral Blood Flow by the Reflexes PROGRESSIVE AND NONPROGRESSIVE HEMORRHAGIC SHOCK Nonprogressive Shock—Compensated Shock Progressive Shock—Caused by Vicious Cycle of Cardiovascular Deterioration Cardiac Depression Vasomotor Failure Blockage of Very Small Vessels by Sludged Blood Increased Capillary Permeability Release of Toxins by Ischemic Tissue Cardiac Depression Caused by Endotoxin Generalized Cellular Deterioration Patchy Areas of Tissue Necrosis Caused by Patchy Blood Flows in Different Organs Acidosis in Shock Positive Feedback Deterioration of Tissues in Shock and Vicious Cycle of Progressive Shock Irreversible Shock Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock HYPOVOLEMIC SHOCK CAUSED BY PLASMA LOSS HYPOVOLEMIC SHOCK CAUSED BY TRAUMA Neurogenic Shock—Increased Vascular Capacity Causes of Neurogenic Shock Anaphylactic Shock and Histamine Shock Septic Shock Special Features of Septic Shock Physiology of Treatment in Shock Replacement Therapy Blood and Plasma Transfusion Dextran Solution as a Plasma Substitute TREATMENT OF NEUROGENIC AND ANAPHYLACTIC SHOCK WITH SYMPATHOMIMETIC DRUGS Other Therapy Treatment by the Head-Down Position Oxygen Therapy Treatment With Glucocorticoids Circulatory Arrest Effect of Circulatory Arrest on the Brain Bibliography Unit V: The Body Fluids and Kidneys Chapter 25: Regulation of Body Fluid Compartments: Extracellular and Intracellular Fluids; Edema Fluid Intake and Output Are Balanced During Steady-State Conditions Daily Intake of Water Daily Loss of Body Water Insensible Water Loss Fluid Loss in Sweat Water Loss in Feces Water Loss by the Kidneys Body Fluid Compartments Intracellular Fluid Compartment Extracellular Fluid Compartment Blood Volume Hematocrit (Packed Red Blood Cell Volume) Constituents of Extracellular and Intracellular Fluids Similar Ionic Composition of Plasma and Interstitial Fluid Intracellular Fluid Constituents Measurement of Body Fluid Compartment Volumes—Indicator-Dilution Principle Determination of Volumes of Specific Body Fluid Compartments Measurement of Total Body Water Measurement of Extracellular Fluid Volume Calculation of Intracellular Volume Measurement of Plasma Volume Calculation of Interstitial Fluid Volume Measurement of Blood Volume Fluid Exchange and Osmotic Equilibrium Between Intracellular and Extracellular Fluid BASIC PRINCIPLES OF OSMOSIS AND OSMOTIC PRESSURE Osmolality and Osmolarity Calculation of the Osmolarity and Osmotic Pressure of a Solution Osmolarity of Body Fluids Corrected Osmolar Activity of Body Fluids Osmotic Equilibrium Between Intracellular and Extracellular Fluids Isotonic, Hypotonic, and Hypertonic Fluids Isosmotic, Hyperosmotic, and Hypo-Osmotic Fluids Osmotic Equilibrium Between Intracellular and Extracellular Fluids Is Rapidly Attained Volume and Osmolality of Extracellular and Intracellular Fluids in Abnormal States Effect of Adding Saline Solution to the Extracellular Fluid Calculation of Fluid Shifts and Osmolarities After Infusion of Hypertonic Saline Solution Glucose and Other Solutions Administered For Nutritive Purposes Clinical Abnormalities of Fluid Volume Regulation: Hyponatremia and Hypernatremia Causes of Hyponatremia: Excess Water or Loss of Sodium Hyponatremia Causes Cell Edema Causes of Hypernatremia: Water Loss or Excess Sodium Hypernatremia Causes Cell Shrinkage Edema: Excess Fluid in the Tissues Intracellular Edema Extracellular Edema Factors That Can Increase Capillary Filtration Lymphedema—Failure of Lymph Vessels to Return Fluid and Protein to the Blood Summary of Causes of Extracellular Edema Edema Caused by Heart Failure Edema Caused by Decreased Kidney Excretion of Salt and Water Edema Caused by Decreased Plasma Proteins Increased Lymph Flow as a Safety Factor Against Edema Washdown of Interstitial Fluid Protein as a Safety Factor Against Edema SAFETY FACTORS THAT NORMALLY PREVENT EDEMA Safety Factor Caused by Low Compliance of the Interstitium in the Negative Pressure Range Importance of Interstitial Gel in Preventing Fluid Accumulation in the Interstitium Importance of Proteoglycan Filaments as a Spacer for Cells and in Preventing Rapid Flow of Fluid in Tissues Increased Lymph Flow as a Safety Factor Against Edema Washdown of Interstitial Fluid Protein as a Safety Factor Against Edema SUMMARY OF SAFETY FACTORS THAT PREVENT EDEMA Fluids in Potential Spaces of the Body Fluid Is Exchanged Between Capillaries and Potential Spaces Lymphatic Vessels Drain Protein From the Potential Spaces Edema Fluid in the Potential Spaces Is Called Effusion Bibliography Chapter 26: The Urinary System: Functional Anatomy and Urine Formation by the Kidneys Multiple Functions of the Kidneys Excretion of Metabolic Waste Products, Foreign Chemicals, Drugs, and Hormone Metabolites Regulation of Water and Electrolyte Balances Regulation of Arterial Pressure Regulation of Acid–Base Balance Regulation of Erythrocyte Production Regulation of 1,25-Dihydroxyvitamin D3 Production Glucose Synthesis PHYSIOLOGIC ANATOMY OF THE KIDNEYS General Organization of the Kidneys and Urinary Tract Renal Blood Supply THE NEPHRON IS THE FUNCTIONAL UNIT OF THE KIDNEY Regional Differences in Nephron Structure: Cortical and Juxtamedullary Nephrons Micturition PHYSIOLOGIC ANATOMY OF THE BLADDER Innervation of the Bladder URINE TRANSPORT FROM THE KIDNEYS THROUGH THE URETERS AND INTO THE BLADDER Pain Sensation in the Ureters and the Ureterorenal Reflex Micturition Reflex Facilitation or Inhibition of Micturition by the Brain Urine Formation Results from Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion FILTRATION, REABSORPTION, AND SECRETION OF DIFFERENT SUBSTANCES Why Are Large Amounts of Solutes Filtered and Then Reabsorbed by the Kidneys? Bibliography Chapter 27: Glomerular Filtration, Renal Blood Flow, and Their Control Glomerular Filtration—The First Step in Urine Formation COMPOSITION OF THE GLOMERULAR FILTRATE GLOMERULAR FILTRATION RATE IS ABOUT 20% OF RENAL PLASMA FLOW Glomerular Capillary Membrane Filterability of Solutes Inversely Related to Their Size Negatively Charged Large Molecules Are Filtered Less Easily Than Positively Charged Molecules of Equal Molecular Size Minimal-Change Nephropathy and Increased Glomerular Permeability to Plasma Proteins Determinants of the Glomerular Filtration Rate INCREASED GLOMERULAR CAPILLARY FILTRATION COEFFICIENT INCREASES GLOMERULAR FILTRATE RATE INCREASED BOWMAN’S CAPSULE HYDROSTATIC PRESSURE DECREASES GLOMERULAR FILTRATION RATE INCREASED GLOMERULAR CAPILLARY COLLOID OSMOTIC PRESSURE DECREASES GLOMERULAR FILTRATION RATE INCREASED GLOMERULAR CAPILLARY HYDROSTATIC PRESSURE INCREASES GLOMERULAR FILTRATION RATE Renal Blood Flow RENAL BLOOD FLOW AND OXYGEN CONSUMPTION Determinants of Renal Blood Flow BLOOD FLOW IN VASA RECTA OF RENAL MEDULLA IS LOW COMPARED WITH RENAL CORTEX FLOW Physiological Control of Glomerular Filtration and Renal Blood Flow STRONG SYMPATHETIC NERVOUS SYSTEM ACTIVATION DECREASES GLOMERULAR FILTRATION RATE HORMONAL AND AUTACOID CONTROL OF RENAL CIRCULATION Norepinephrine, Epinephrine, and Endothelin Constrict Renal Blood Vessels and Decrease Glomerular Filtration Rate Angiotensin II Preferentially Constricts Efferent Arterioles in Most Physiological Conditions Endothelial Derived Nitric Oxide Decreases Renal Vascular Resistance and Increases Glomerular Filtration Rate Prostaglandins and Bradykinin Decrease Renal Vascular Resistance and Tend to Increase Glomerular Filtration Rate Autoregulation of Glomerular Filtration Rate and Renal Blood Flow Importance of Glomerular Filtration Rate Autoregulation in Preventing Extreme Changes in Renal Excretion TUBULOGLOMERULAR FEEDBACK AND AUTOREGULATION OF GLOMERULAR FILTRATION RATE Decreased Macula Densa Sodium Chloride Causes Dilation of Afferent Arterioles and Increased Renin Release MYOGENIC AUTOREGULATION OF RENAL BLOOD FLOW AND GLOMERULAR FILTRATION RATE Bibliography Chapter 28: Renal Tubular Reabsorption and Secretion Tubular Reabsorption is Quantitatively Large and Highly Selective Tubular Reabsorption Includes Passive and Active Mechanisms Active Transport Solutes Can Be Transported Through Epithelial Cells or Between Cells Primary Active Transport Through the Tubular Membrane Linked to Hydrolysis of Adenosine Triphosphatase Secondary Active Reabsorption Through the Tubular Membrane Secondary Active Secretion Into the Tubules Pinocytosis Is an Active Transport Mechanism for Reabsorption of Proteins Transport Maximum for Substances That Are Actively Reabsorbed Transport Maximums for Actively Secreted Substances Substances That Are Actively Transported but Do Not Exhibit a Transport Maximum PASSIVE WATER REABSORPTION BY OSMOSIS COUPLED MAINLY TO SODIUM REABSORPTION REABSORPTION OF CHLORIDE, UREA, AND OTHER SOLUTES BY PASSIVE DIFFUSION Reabsorption and Secretion Along Different Parts of the Nephron Proximal Tubular Reabsorption Proximal Tubules Have High Capacity for Active and Passive Reabsorption Concentrations of Solutes Along Proximal Tubules Secretion of Organic Acids and Bases by Proximal Tubules SOLUTE AND WATER TRANSPORT IN LOOPS OF HENLE Distal Tubules LATE DISTAL TUBULES AND CORTICAL COLLECTING TUBULES Principal Cells Reabsorb Sodium and Secrete Potassium Intercalated Cells Can Secrete or Reabsorb Hydrogen, Bicarbonate, and Potassium Ions Medullary Collecting Ducts SUMMARY OF CONCENTRATIONS OF DIFFERENT SOLUTES IN DIFFERENT TUBULAR SEGMENTS Tubular Fluid/Plasma Inulin Concentration Ratio Can Be Used to Assess Water Reabsorption by Renal Tubules Regulation of Tubular Reabsorption GLOMERULOTUBULAR BALANCE—REABSORPTION RATE INCREASES IN RESPONSE TO INCREASED TUBULAR LOAD PERITUBULAR CAPILLARY AND RENAL INTERSTITIAL FLUID PHYSICAL FORCES Normal Values for Physical Forces and Reabsorption Rate Regulation of Peritubular Capillary Physical Forces Renal Interstitial Hydrostatic and Colloid Osmotic Pressures EFFECT OF ARTERIAL PRESSURE ON URINE OUTPUT—PRESSURE NATRIURESIS AND PRESSURE DIURESIS HORMONAL CONTROL OF TUBULAR REABSORPTION Aldosterone Stimulates Renal Sodium Reabsorption and Potassium Secretion Angiotensin II Increases Sodium and Water Reabsorption Antidiuretic Hormone Increases Water Reabsorption Atrial Natriuretic Peptide Decreases Sodium and Water Reabsorption Parathyroid Hormone Increases Calcium Reabsorption SYMPATHETIC NERVOUS SYSTEM ACTIVATION INCREASES SODIUM REABSORPTION Use of Clearance Methods to Quantify Kidney Function INULIN CLEARANCE CAN BE USED TO ESTIMATE GLOMERULAR FILTRATION RATE CREATININE CLEARANCE AND PLASMA CREATININE CONCENTRATION CAN BE USED TO ESTIMATE GLOMERULAR FILTRATION RATE PARA-AMINOHIPPURIC ACID CLEARANCE CAN BE USED TO ESTIMATE RENAL PLASMA FLOW FILTRATION FRACTION IS CALCULATED FROM GFR DIVIDED BY RPF CALCULATION OF TUBULAR REABSORPTION OR SECRETION FROM RENAL CLEARANCES Bibliography Chapter 29: Urine Concentration and Dilution; Regulation of Extracellular Fluid Osmolarity and Sodium Concentration Kidneys Excrete Excess Water by Forming Dilute Urine ANTIDIURETIC HORMONE CONTROLS URINE CONCENTRATION RENAL MECHANISMS FOR EXCRETING DILUTE URINE Tubular Fluid Remains Isosmotic in Proximal Tubules Tubular Fluid Is Diluted in the Ascending Loop of Henle Tubular Fluid in Distal and Collecting Tubules Is Further Diluted in Absence of ADH Kidneys Conserve Water by Excreting Concentrated Urine EXCRETING CONCENTRATED URINE REQUIRES HIGH ADH LEVELS AND HYPEROSMOTIC RENAL MEDULLA Countercurrent Multiplier Mechanism Produces Hyperosmotic Renal Medullary Interstitium Loop of Henle Characteristics That Cause Solutes to be Trapped in the Renal Medulla Steps Involved in Causing Hyperosmotic Renal Medullary Interstitium ROLE OF DISTAL TUBULE AND COLLECTING DUCTS IN EXCRETING CONCENTRATED URINE UREA CONTRIBUTES TO HYPEROSMOTIC RENAL MEDULLARY INTERSTITIUM AND FORMATION OF CONCENTRATED URINE Recirculation of Urea from Collecting Duct to Loop of Henle Contributes to Hyperosmotic Renal Medulla COUNTERCURRENT EXCHANGE IN VASA RECTA PRESERVES HYPEROSMOLARITY OF RENAL MEDULLA Increased Medullary Blood Flow Reduces Urine-Concentrating Ability SUMMARY OF URINE-CONCENTRATING MECHANISM AND CHANGES IN OSMOLARITY IN DIFFERENT TUBULAR SEGMENTS Proximal Tubule Descending Loop of Henle Thin Ascending Loop of Henle Thick Ascending Loop of Henle Early Distal Tubule Late Distal Tubule and Cortical Collecting Tubules Inner Medullary Collecting Ducts Control of Extracellular Fluid Osmolarity and Sodium Concentration Estimating Plasma Osmolarity From Plasma Sodium Concentration Osmoreceptor­ADH Feedback System ADH SYNTHESIS IN SUPRAOPTIC AND PARAVENTRICULAR NUCLEI OF HYPOTHALAMUS AND ADH RELEASE FROM POSTERIOR PITUITARY STIMULATION OF ADH RELEASE BY DECREASED ARTERIAL PRESSURE AND/OR DECREASED BLOOD VOLUME Quantitative Importance of Osmolarity and Cardiovascular Reflexes in Stimulating ADH Secretion Other Stimuli for ADH Secretion Importance of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration CENTRAL NERVOUS SYSTEM CENTERS FOR THIRST Stimuli for Thirst THRESHOLD FOR OSMOLAR STIMULUS OF DRINKING INTEGRATED RESPONSES OF OSMORECEPTOR-ADH AND THIRST MECHANISMS Bibliography Chapter 30: Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume Regulation of Extracellular Fluid Potassium Concentration and Potassium Excretion REGULATION OF INTERNAL POTASSIUM DISTRIBUTION Insulin Stimulates Potassium Uptake Into Cells Aldosterone Increases Potassium Uptake Into Cells β-Adrenergic Stimulation Increases Cellular Uptake of Potassium Acid–Base Abnormalities Can Cause Changes in Potassium Distribution Cell Lysis Causes Increased Extracellular Potassium Concentration Strenuous Exercise Can Cause Hyperkalemia by Releasing Potassium From Skeletal Muscle Increased Extracellular Fluid Osmolarity Causes Redistribution of Potassium From Cells to Extracellular Fluid OVERVIEW OF RENAL POTASSIUM EXCRETION Variable Potassium Secretion in Distal and Collecting Tubules Mediates Most Daily Changes in Potassium Excretion PRINCIPAL CELLS OF LATE DISTAL AND CORTICAL COLLECTING TUBULES SECRETE POTASSIUM Control of Potassium Secretion by Principal Cells Intercalated Cells Can Reabsorb or Secrete Potassium SUMMARY OF MAJOR FACTORS THAT REGULATE POTASSIUM SECRETION Increased Extracellular Fluid Potassium Concentration Stimulates Potassium Secretion Aldosterone Stimulates Potassium Secretion Increased Extracellular Potassium Ion Concentration Stimulates Aldosterone Secretion Blockade of Aldosterone Feedback System Greatly Impairs Potassium Regulation Increased Distal Tubular Flow Rate Stimulates Potassium Secretion Acute Acidosis Decreases Potassium Secretion Regulation of Renal Calcium Excretion and Extracellular Calcium Ion Concentration CONTROL OF CALCIUM EXCRETION BY THE KIDNEYS Proximal Tubular Calcium Reabsorption Loop of Henle and Distal Tubule Calcium Reabsorption Regulation of Tubular Calcium Reabsorption Regulation of Renal Phosphate Excretion Regulation of Renal Magnesium Excretion and Extracellular Magnesium Ion Concentration Integration of Renal Mechanisms for Control of Extracellular Fluid SODIUM INTAKE AND EXCRETION ARE BALANCED UNDER STEADY-STATE CONDITIONS SODIUM EXCRETION IS CONTROLLED BY ALTERING GLOMERULAR FILTRATION OR TUBULAR SODIUM REABSORPTION RATES Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance Pressure Natriuresis and Diuresis: Key Components of A Renal–Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure EFFECTIVENESS OF BLOOD VOLUME AND EXTRACELLULAR FLUID VOLUME REGULATION Distribution of Extracellular Fluid Between Interstitial Spaces and Vascular System Nervous and Hormonal Factors Increase Effectiveness of Renal–Body Fluid Feedback Control SYMPATHETIC NERVOUS SYSTEM CONTROL OF RENAL EXCRETION: ARTERIAL BARORECEPTOR AND LOW-PRESSURE STRETCH RECEPTOR REFLEXES ROLE OF ANGIOTENSIN II IN CONTROLLING RENAL EXCRETION Importance of Changes in Angiotensin II in Regulating Sodium Balance and Altering Pressure Natriuresis ROLE OF ALDOSTERONE IN CONTROLLING RENAL EXCRETION ROLE OF ANTIDIURETIC HORMONE IN CONTROLLING RENAL WATER EXCRETION ROLE OF ATRIAL NATRIURETIC PEPTIDE IN CONTROLLING RENAL EXCRETION Integrated Responses to Changes in Sodium Intake High Sodium Intake Suppresses Antinatriuretic Systemsand Activates Natriuretic Systems Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume INCREASED BLOOD VOLUME AND EXTRACELLULAR FLUID VOLUME CAUSED BY HEART DISEASES INCREASED BLOOD VOLUME CAUSED BY INCREASED VASCULAR CAPACITY Conditions That Cause Large Increases in Extracellular Fluid Volume With Normal or Reduced Blood Volume NEPHROTIC SYNDROME—LOSS OF PLASMA PROTEINS IN URINE AND SODIUM RETENTION BY THE KIDNEYS LIVER CIRRHOSIS—DECREASED SYNTHESIS OF PLASMA PROTEINS BY THE LIVER AND SODIUM RETENTION BY THE KIDNEYS Bibliography Chapter 31: Acid–Base Regulation Hydrogen Ion Concentration is Precisely Regulated Acids and Bases—Definitions and Meanings Strong and Weak Acids and Bases Normal H+ Concentration and pH of Body Fluids and Changes That Occur in Acidosis and Alkalosis Defending Against Changes in H+ Concentration: Buffers, Lungs, and Kidneys Buffering of H+ in the Body Fluids Bicarbonate Buffer System Phosphate Buffer System Proteins are Important Intracellular Buffers Respiratory Regulation of Acid–­Base Balance PULMONARY EXPIRATION OF CO2 BALANCES METABOLIC FORMATION OF CO2 INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES pH INCREASED H+ CONCENTRATION STIMULATES ALVEOLAR VENTILATION Feedback Control of H+ Concentration by the Respiratory System Efficiency of Respiratory Control of H+ Concentration Buffering Power of the Respiratory System Impairment of Lung Function Can Cause Respiratory Acidosis Renal Control of Acid–Base Balance Secretion of H+ and Reabsorption of HCO3− by the Renal Tubules H+ SECRETED BY SECONDARY ACTIVE TRANSPORT IN EARLY TUBULAR SEGMENTS FILTERED HCO3− IS REABSORBED BY INTERACTION WITH H+ IN THE TUBULES HCO3− Is Titrated Against H+ in the Tubules PRIMARY ACTIVE SECRETION OF H+ IN THE INTERCALATED CELLS OF LATE DISTAL AND COLLECTING TUBULES Combination of Excess H+ with Phosphate and Ammonia Buffers In the Tubule Generates “New” HCO3− PHOSPHATE BUFFER SYSTEM CARRIES EXCESS H+ INTO THE URINE AND GENERATES NEW HCO3− EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO3− BY AMMONIA BUFFER SYSTEM Chronic Acidosis Increases NH4+ Excretion Quantifying Renal Acid–Base Excretion Regulation of Renal Tubular H+ Secretion Renal Correction of Acidosis—Increased Excretion of H+ and Addition of HCO3− to the Extracellular Fluid ACIDOSIS DECREASES HCO3−/H+ RATIO IN RENAL TUBULAR FLUID Renal Correction of Alkalosis—Decreased Tubular Secretion of H+ and Increased Excretion of HCO3− ALKALOSIS INCREASES HCO3−/H+ RATIO IN RENAL TUBULAR FLUID Bibliography Chapter 32: Diuretics and Kidney Diseases DIURETICS AND THEIR MECHANISMS OF ACTION Osmotic Diuretics Decrease Water Reabsorption by Increasing Osmotic Pressure of Tubular Fluid Loop Diuretics Decrease Sodium-Chloride-Potassium Reabsorption in the Thick Ascending Loop of Henle Thiazide Diuretics Inhibit Sodium-Chloride Reabsorption in the Early Distal Tubule Carbonic Anhydrase Inhibitors Block Sodium Bicarbonate Reabsorption Mineralocorticoid Receptor Antagonists Decrease Sodium Reabsorption From and Potassium Secretion Into the Collecting Tubules Sodium Channel Blockers Decrease Sodium Reabsorption in the Collecting Tubules KIDNEY DISEASES ACUTE KIDNEY INJURY PRERENAL ACUTE KIDNEY INJURY CAUSED BY DECREASED BLOOD FLOW TO THE KIDNEY INTRARENAL ACUTE KIDNEY INJURY CAUSED BY ABNORMALITIES IN THE KIDNEY Acute Kidney Injury Caused by Glomerulonephritis Tubular Necrosis as a Cause of Acute Kidney Injury Acute Tubular Necrosis Caused by Severe Renal Ischemia Acute Tubular Necrosis Caused by Toxins or Medications POSTRENAL ACUTE KIDNEY INJURY CAUSED BY ABNORMALITIES OF THE LOWER URINARY TRACT PHYSIOLOGICAL EFFECTS OF ACUTE KIDNEY INJURY CHRONIC KIDNEY DISEASE IS OFTEN ASSOCIATED WITH IRREVERSIBLE LOSS OF FUNCTIONAL NEPHRONS VICIOUS CYCLE OF CHRONIC KIDNEY DISEASE LEADING TO END-STAGE RENAL DISEASE INJURY TO RENAL BLOOD VESSELS AS A CAUSE OF CHRONIC KIDNEY DISEASE INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS INJURY TO THE RENAL INTERSTITIUM AS A CAUSE OF CHRONIC KIDNEY DISEASE—INTERSTITIAL NEPHRITIS NEPHROTIC SYNDROME—EXCRETION OF PROTEIN IN THE URINE NEPHRON FUNCTION IN CHRONIC KIDNEY DISEASE Loss of Functional Nephrons Requires Surviving Nephrons to Excrete More Water and Solutes Isosthenuria—Inability of the Kidney to Concentrate or Dilute the Urine Bibliography Unit VI: Blood Cells, Immunity, and Blood Coagulation Chapter 33: Red Blood Cells, Anemia, and Polycythemia Red Blood Cells (Erythrocytes) Shape and Size of Red Blood Cells Concentration of Red Blood Cells in the Blood Quantity of Hemoglobin in the Cells PRODUCTION OF RED BLOOD CELLS Areas of the Body That Produce Red Blood Cells Genesis of Blood Cells Multipotential Hematopoietic Stem Cells, Growth Inducers, and Differentiation Inducers Stages of Differentiation of Red Blood Cells Erythropoietin Regulates Red Blood Cell Production Tissue Oxygenation—Essential Regulator of Red Blood Cell Production Hypoxia Increases Formation of Erythropoietin Which Stimulates Red Blood Cell Production Erythropoietin Is Formed Mainly in the Kidneys Erythropoietin Stimulates Production of Proerythroblasts From Hematopoietic Stem Cells Maturation of Red Blood Cells Requires Vitamin B12 (Cyanocobalamin) and Folic Acid Maturation Failure Anemia Caused by Poor Absorption of Vitamin B12 From the Gastrointestinal Tract—Pernicious Anemia Maturation Failure Anemia Caused by Folic Acid (Pteroylglutamic Acid) Deficiency HEMOGLOBIN FORMATION Hemoglobin Combines Reversibly With Oxygen IRON METABOLISM Transport and Storage of Iron Daily Loss of Iron Absorption of Iron From the Intestinal Tract Regulation of Total Body Iron by Controlling Absorption Rate LIFE SPAN OF RED BLOOD CELLS IS ABOUT 120 DAYS Destruction of Hemoglobin by Macrophages Anemias Blood Loss Anemia Aplastic Anemia Due to Bone Marrow Dysfunction Megaloblastic Anemia Hemolytic Anemia EFFECTS OF ANEMIA ON CIRCULATORY SYSTEM FUNCTION Polycythemia Secondary Polycythemia Polycythemia Vera (Erythremia) EFFECT OF POLYCYTHEMIA ON FUNCTION OF THE CIRCULATORY SYSTEM Bibliography Chapter 34: Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation Leukocytes (White Blood Cells) GENERAL CHARACTERISTICS OF LEUKOCYTES Types of White Blood Cells Concentrations of Different White Blood Cells in Blood GENESIS OF WHITE BLOOD CELLS LIFE SPAN OF WHITE BLOOD CELLS Neutrophils and Macrophages Defend Against Infections White Blood Cells Enter the Tissue Spaces by Diapedesis White Blood Cells Move Through Tissue Spaces by Ameboid Motion White Blood Cells Are Attracted to Inflamed Tissue Areas by Chemotaxis Phagocytosis Phagocytosis by Neutrophils Phagocytosis by Macrophages Once Phagocytized, Most Particles Are Digested by Intracellular Enzymes Neutrophils and Macrophages Can Kill Bacteria Monocyte-Macrophage Cell System (Reticuloendothelial System) Tissue Macrophages in Skin and Subcutaneous Tissues (Histiocytes) Macrophages in Lymph Nodes Alveolar Macrophages in Lungs Macrophages (Kupffer Cells) in Liver Sinusoids Macrophages of Spleen and Bone Marrow INFLAMMATION: ROLE OF NEUTROPHILS AND MACROPHAGES Inflammation Walling-Off Effect of Inflammation Macrophage and Neutrophil Responses During Inflammation Tissue Macrophages Provide First Line of Defense Against Infection Neutrophil Invasion of the Inflamed Area Is a Second Line of Defense Acute Increase in the Number of Neutrophils in Blood—Neutrophilia Second Macrophage Invasion Into the Inflamed Tissue Is a Third Line of Defense Increased Production of Granulocytes and Monocytes by Bone Marrow Is a Fourth Line of Defense Feedback Control of Macrophage and Neutrophil Responses Formation of Pus Eosinophils Basophils Leukopenia Leukemias Effects of Leukemia on the Body Bibliography Chapter 35: Resistance of the Body to Infection: II. Immunity and Allergy Acquired (Adaptive) Immunity BASIC TYPES OF ACQUIRED IMMUNITY—HUMORAL AND CELL-MEDIATED BOTH TYPES OF ACQUIRED IMMUNITY ARE INITIATED BY ANTIGENS LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY T and B Lymphocytes Promote Cell­Mediated and Humoral Immunity PREPROCESSING OF T AND BLYMPHOCYTES Thymus Gland Preprocesses T Lymphocytes Liver and Bone Marrow Preprocess B Lymphocytes T LYMPHOCYTES AND B-LYMPHOCYTEANTIBODIES REACT AGAINST SPECIFICANTIGENS—ROLE OF LYMPHOCYTECLONES Millions of Specific Types of Lymphocytes Are Stored in Lymphoid Tissue ORIGIN OF THE MANY CLONES OF LYMPHOCYTES MECHANISM FOR ACTIVATING LYMPHOCYTE CLONES Role of Macrophages in the Activation Process Role of T Cells in Activation of B Lymphocytes. Most antigens activate both T lymphocytes and B lymphocytes at the same time. So... Specific Attributes of The B­Lymphocyte System—Humoral Immunity and Antibodies Antibody Formation by Plasma Cells Formation of Memory Cells Enhances Antibody Response to Subsequent Antigen Exposure Generation of Lifelong Immunity by Plasma Cells Nature of Antibodies Specificity of Antibodies Five General Classes of Antibodies Mechanisms of Action of Antibodies Direct Action of Antibodies on Invading Agents COMPLEMENT SYSTEM FOR ANTIBODY ACTION Classical Pathway Special Attributes of T­Lymphocyte System—Activated T Cells and Cell­Mediated Immunity Release of Activated T Cells From Lymphoid Tissue and Formation of Memory Cells Antigen­Presenting Cells, Major Histocompatibility Complex Proteins, and Antigen Receptors on T Lymphocytes Different Types of T Cells and Their Functions T­Helper Cells Are the Most Numerous T Cells Specific Regulatory Functions of Lymphokines Stimulation of Growth and Proliferation of Cytotoxic T Cells and Regulatory T Cells Stimulation of B­Cell Growth and Differentiation to Form Plasma Cells and Antibodies Activation of the Macrophage System Feedback Stimulatory Effect on T­Helper Cells Cytotoxic T Cells Are Killer Cells Regulatory T Cells TOLERANCE OF ACQUIRED IMMUNITY SYSTEM TO THE BODY’S OWN TISSUES—ROLE OF PREPROCESSING IN THYMUS AND BONE MARROW Most Tolerance Results From Clone Selection During Preprocessing Failure of the Tolerance Mechanism Causes Autoimmune Diseases IMMUNIZATION BY INJECTION OF ANTIGENS Passive Immunity Allergy and Hypersensitivity ALLERGY CAUSED BY ACTIVATED T CELLS: DELAYED-REACTION ALLERGY ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IgE ANTIBODIES Anaphylaxis—Widespread Allergic Reaction Urticaria—Localized Anaphylactoid Reactions Hay Fever Asthma Bibliography Chapter 36: Blood Types; Transfusion; and Tissue and Organ Transplantation Antigenicity Causes Immune Reactions of Blood Multiplicity of Antigens in the Blood Cells O­A­B Blood Types A and B Antigens—Agglutinogens Major O-A-B Blood Types Genetic Determination of the Agglutinogens Relative Frequencies of Different Blood Types Agglutinins Titer of Agglutinins at Different Ages Origin of Agglutinins in Plasma AGGLUTINATION PROCESS IN TRANSFUSION REACTIONS Acute Hemolysis Occurs in Some Transfusion Reactions Blood Typing Rh Blood Types Rh Antigens—Rh-Positive and Rh-Negative Rh Immune Response Formation of Anti-Rh Agglutinins Characteristics of Rh Transfusion Reactions Erythroblastosis Fetalis (Hemolytic Disease of the Newborn) Incidence of Erythroblastosis Fetalis Effect of Mother’s Antibodies on the Fetus Clinical Picture of Erythroblastosis Treatment of Neonates With Erythroblastosis Fetalis Prevention of Erythroblastosis Fetalis Transfusion Reactions Resulting From Mismatched Blood Types Acute Kidney Failure After Transfusion Reactions Transplantation of Tissues and Organs Autografts, Isografts, Allografts, and Xenografts Transplantation of Cellular Tissues ATTEMPTS TO OVERCOME IMMUNE REACTIONS IN TRANSPLANTED TISSUE Tissue Typing—Human Leukocyte Antigen Complex of Antigens Prevention of Graft Rejection by Suppressing the Immune System Bibliography Chapter 37: Hemostasis and Blood Coagulation HEMOSTASIS EVENTS VASCULAR CONSTRICTION FORMATION OF THE PLATELET PLUG Physical and Chemical Characteristics Mechanism of Platelet Plug Formation Importance of Platelet Mechanism for Closing Vascular Holes BLOOD COAGULATION IN THE RUPTURED VESSEL FIBROUS ORGANIZATION OR DISSOLUTION OF BLOOD CLOTS MECHANISM OF BLOOD COAGULATION GENERAL MECHANISM CONVERSION OF PROTHROMBIN TO THROMBIN Prothrombin and Thrombin CONVERSION OF FIBRINOGEN TO FIBRIN—FORMATION OF THE CLOT Fibrinogen Formed in the Liver Essential for Clot Formation Action of Thrombin on Fibrinogen to Form Fibrin Blood Clot Clot Retraction and Expression of Serum POSITIVE FEEDBACK OF CLOT FORMATION INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR Extrinsic Pathway for Initiating Clotting Intrinsic Pathway for Initiating Clotting Role of Calcium Ions in the Intrinsic and Extrinsic Pathways Interaction Between Extrinsic and Intrinsic Pathways—Summary of Blood-­Clotting Initiation Intravascular Anticoagulants Prevent Blood Clotting in the Normal Vascular System Endothelial Surface Factors Antithrombin Action of Fibrin and Antithrombin III Heparin PLASMIN CAUSES LYSIS OF BLOOD CLOTS Activation of Plasminogen to Form Plasmin, Then Clot Lysis CONDITIONS THAT CAUSE EXCESSIVE BLEEDING IN HUMANS DECREASED PROTHROMBIN, FACTOR VII, FACTOR IX, AND FACTOR X CAUSED BY VITAMIN K DEFICIENCY HEMOPHILIA THROMBOCYTOPENIA THROMBOEMBOLIC CONDITIONS Thrombi and Emboli Causes of Thromboembolic Conditions Use of Tissue Plasminogen Activator in Treating Intravascular Clots FEMORAL VENOUS THROMBOSIS AND MASSIVE PULMONARY EMBOLISM DISSEMINATED INTRAVASCULAR COAGULATION ANTICOAGULANTS FOR CLINICAL USE COUMARINS AS ANTICOAGULANTS HEPARIN—INTRAVENOUS ANTICOAGULANT PREVENTION OF BLOOD COAGULATION OUTSIDE THE BODY BLOOD COAGULATION TESTS BLEEDING TIME CLOTTING TIME PROTHROMBIN TIME AND INTERNATIONAL NORMALIZED RATIO Bibliography Unit VII: Respiration Chapter 38: Pulmonary Ventilation MECHANICS OF PULMONARY VENTILATION MUSCLES THAT CAUSE LUNG EXPANSION AND CONTRACTION PRESSURES THAT CAUSE MOVEMENT OF AIR IN AND OUT OF THE LUNGS Pleural Pressure and Its Changes During Respiration Alveolar Pressure—Air Pressure Inside the Lung Alveoli Transpulmonary Pressure—Difference between Alveolar and Pleural Pressures Compliance of the Lungs Compliance Diagram of the Lungs Surfactant, Surface Tension, and Collapse of the Alveoli Principle of Surface Tension Surfactant and Its Effect on Surface Tension EFFECT OF THE THORACIC CAGE ON LUNG EXPANSIBILITY Compliance of Thorax and Lungs Together PULMONARY VOLUMES AND CAPACITIES RECORDING CHANGES IN PULMONARY VOLUME—SPIROMETRY Pulmonary Volumes Pulmonary Capacities ABBREVIATIONS AND SYMBOLS USED IN PULMONARY FUNCTION STUDIES DETERMINATION OF FUNCTIONAL RESIDUAL CAPACITY, RESIDUAL VOLUME, AND TOTAL LUNG CAPACITY—HELIUM DILUTION METHOD MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME ALVEOLAR VENTILATION DEAD SPACE AND ITS EFFECT ON ALVEOLAR VENTILATION RATE OF ALVEOLAR VENTILATION Bibliography Chapter 39: Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid PHYSIOLOGICAL ANATOMY OF THE PULMONARY CIRCULATORY SYSTEM Pulmonary Vessels Bronchial Vessels Lymphatics PRESSURES IN THE PULMONARY SYSTEM Pressures in the Right Ventricle Pressures in the Pulmonary Artery Pulmonary Capillary Pressure Left Atrial and Pulmonary Venous Pressures BLOOD VOLUME OF THE LUNGS Lungs Serve as a Blood Reservoir Cardiac Pathology May Shift Blood From Systemic Circulation to Pulmonary Circulation BLOOD FLOW THROUGH THE LUNGS AND ITS DISTRIBUTION Decreased Alveolar Oxygen Reduces Local Alveolar Blood Flow and Regulates Pulmonary Blood Flow Distribution EFFECT OF HYDROSTATIC PRESSURE GRADIENTS IN THE LUNGS ON REGIONAL PULMONARY BLOOD FLOW Zones 1, 2, and 3 of Pulmonary Blood Flow Zone 1 Blood Flow Occurs Only Under Abnormal Conditions Exercise Increases Blood Flow Through All Parts of the Lungs Increased Cardiac Output During Heavy Exercise Is Normally Accommodated by the Pulmonary Circulation Without Large Increases in Pulmonary Artery Pressure Function of Pulmonary Circulation When Left Atrial Pressure Rises as a Result of Left-Sided Heart Failure PULMONARY CAPILLARY DYNAMICS Pulmonary Capillary Pressure Length of Time Blood Stays in the Pulmonary Capillaries Capillary Exchange of Fluid in the Lungs and Pulmonary Interstitial Fluid Dynamics Interrelationships Between Interstitial Fluid Pressure and Other Pressures in the Lung Negative Pulmonary Interstitial Pressure and Mechanism for Keeping Alveoli Dry FLUID IN THE PLEURAL CAVITY Negative Pressure in Pleural Fluid Pleural Effusion—Collection of Large Amounts of Free Fluid in the Pleural Space Bibliography Chapter 40: Principles of Gas Exchange; Diffusion of Oxygen and Carbon Dioxide Through the Respiratory Membrane Compositions of Alveolar Air and Atmospheric Air are Different Air Is Humidified in the Respiratory Passages Alveolar Air Is Slowly Renewed by Atmospheric Air Slow Replacement of Alveolar Air Helps Stabilize Respiratory Control Oxygen Concentration and Partial Pressure in Alveoli CO2 Concentration and Partial Pressure in Alveoli DIFFUSION OF GASES THROUGH THE RESPIRATORY MEMBRANE Respiratory Unit Respiratory Membrane Factors Affecting Rate of Gas Diffusion Through the Respiratory Membrane Diffusing Capacity of the Respiratory Membrane Diffusing Capacity for Oxygen Increased Oxygen Diffusing Capacity During Exercise Diffusing Capacity for Carbon Dioxide Bibliography Chapter 41: Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids TRANSPORT OF OXYGEN FROM THE LUNGS TO THE BODY TISSUES DIFFUSION OF OXYGEN FROM THE ALVEOLI TO THE PULMONARY CAPILLARY BLOOD Uptake of Oxygen by the Pulmonary Blood During Exercise TRANSPORT OF OXYGEN IN ARTERIAL BLOOD DIFFUSION OF OXYGEN FROM THE PERIPHERAL CAPILLARIES INTO THE TISSUE FLUID Increasing Blood Flow Raises Interstitial Fluid Po2 Increasing Tissue Metabolism Decreases Interstitial Fluid Po2 DIFFUSION OF OXYGEN FROM PERIPHERAL CAPILLARIES TO TISSUE CELLS DIFFUSION OF CO2 FROM PERIPHERAL TISSUE CELLS INTO CAPILLARIES AND FROM PULMONARY CAPILLARIES INTO ALVEOLI Effect of Tissue Metabolism and Tissue Blood Flow Rate on Interstitial Pco2 ROLE OF HEMOGLOBIN IN OXYGEN TRANSPORT Reversible Combination of O2 With Hemoglobin Oxygen-Hemoglobin Dissociation Curve Maximum Amount of Oxygen That Can Combine With the Hemoglobin of the Blood Amount of Oxygen Released From Hemoglobin When Systemic Arterial Blood Flows Through Tissues Transport of Oxygen Is Markedly Increased During Strenuous Exercise Utilization Coefficient Hemoglobin “Buffers” Tissue Po2 Hemoglobin Helps Maintain Nearly Constant Po2 in the Tissues When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue Po2 Factors That Shift the Oxygen-Hemoglobin Dissociation Curve—Their Importance for Oxygen Transport Increased Delivery of Oxygen to Tissues When CO2 and H+ Shift the Oxygen-Hemoglobin Dissociation Curve—the Bohr Effect Effect of BPG to Cause Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve During Exercise Metabolic Use of Oxygen by Cells Effect of Intracellular Po2 on Oxygen Usage Rate Effect of Diffusion Distance From the Capillary to the Cell on Oxygen Usage Effect of Blood Flow on Metabolic Use of Oxygen Transport of CO2 in Blood CHEMICAL FORMS IN WHICH CO2 IS TRANSPORTED Transport of CO2 in a Dissolved State Transport of CO2 in the Form of Bicarbonate Ion Carbonic Anhydrase Catalyzes the Reaction of CO2 With Water in Red Blood Cells Dissociation of Carbonic Acid Into Bicarbonate and Hydrogen Ions Transport of CO2 in Combination With Hemoglobin and Plasma Proteins—Carbaminohemoglobin Carbon Dioxide Dissociation Curve When Oxygen Binds With Hemoglobin, CO2 Is Released (the Haldane Effect) to Increase CO2 Transport Respiratory Exchange Ratio Bibliography Chapter 42: Regulation of Respiration Respiratory Center DORSAL RESPIRATORY GROUP OF NEURONS CONTROLS INSPIRATION AND RESPIRATORY RHYTHM Rhythmical Inspiratory Discharges From the Dorsal Respiratory Group Inspiratory “Ramp” Signal PNEUMOTAXIC CENTER LIMITS DURATION OF INSPIRATION AND INCREASES RESPIRATORY RATE VENTRAL RESPIRATORY GROUP OF NEURONS—FUNCTIONS IN BOTH INSPIRATION AND EXPIRATION LUNG INFLATION SIGNALS LIMIT INSPIRATION—THE HERING-BREUER INFLATION REFLEX CONTROL OF OVERALL RESPIRATORY CENTER ACTIVITY Chemical Control of Respiration Direct Control of Respiratory Center Activity by Co2 and H+ Chemosensitive Area of the Respiratory Center Beneath the Medulla’s Ventral Surface Excitation of the Chemosensitive Neurons by H+ Is Likely the Primary Stimulus CO2 Indirectly Stimulates the Chemosensitive Neurons Attenuated Stimulatory Effect of CO2 After the First 1 to 2 Days Quantitative Effects of Blood Pco2 and H+ Concentration on Alveolar Ventilation Changes in O2 Have Little Direct Effect on Control of the Respiratory Center Peripheral Chemoreceptor System—Role of Oxygen in Respiratory Control Decreased Arterial Oxygen Stimulates the Chemoreceptors Basic Mechanism of Stimulation of the Chemoreceptors by O2 Deficiency. The exact means whereby low Po2 excites the nerve endings... Increased CO2 and H+ Concentration Stimulates the Chemoreceptors. An increase in CO2 or H+ concentration also excites the chemor... Effect of Low Arterial Po2 to Stimulate Alveolar Ventilation When Arterial CO2 and H+ Concentrations Remain Normal Chronic Breathing of Low O2 Stimulates Respiration Even More—The Phenomenon of “Acclimatization” Composite Effects of Pco2, pH, and Po2 on Alveolar Ventilation Regulation of Respiration During Exercise Interrelationship Between Chemical and Nervous Factors in Controlling Respiration During Exercise Neurogenic Control of Ventilation During Exercise May Be Partly a Learned Response Bibliography Chapter 43: Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy Useful Methods for Studying Respiratory Abnormalities Study of Blood Gases and Blood ph Determination of Blood pH Determination of Blood CO2 Determination of Blood Po2 MEASUREMENT OF MAXIMUM EXPIRATORY FLOW Abnormalities of the Maximum Expiratory Flow-Volume Curve FORCED EXPIRATORY VITAL CAPACITY AND FORCED EXPIRATORY VOLUME PATHOPHYSIOLOGY OF SPECIFIC PULMONARY ABNORMALITIES Chronic Pulmonary Emphysema PNEUMONIA—LUNG INFLAMMATION AND FLUID IN ALVEOLI Atelectasis—Collapse of the Alveoli Airway Obstruction Causes Lung Collapse Lack of “Surfactant” as a Cause of Lung Collapse ASTHMA—SPASMODIC CONTRACTION OF SMOOTH MUSCLES IN BRONCHIOLES Tuberculosis Hypoxia and Oxygen Therapy Inadequate Tissue Capability to Use Oxygen Effects of Hypoxia on the Body OXYGEN THERAPY IN DIFFERENT TYPES OF HYPOXIA Cyanosis Hypercapnia—Excess Carbon Dioxide in the Body Fluids Dyspnea Artificial Respiration Resuscitator Tank Respirator (the “Iron Lung”) Effect of the Resuscitator and the Tank Respirator on Venous Return Bibliography Unit VIII: Aviation, Space, and Deep-Sea Diving Physiology Chapter 44: Aviation, High Altitude, and Space Physiology EFFECTS OF LOW OXYGEN PRESSURE ON THE BODY Barometric Pressures at Different Altitudes Alveolar Po2 at Different Elevations Carbon Dioxide and Water Vapor Decrease the Alveolar Oxygen Alveolar Po2 at Different Altitudes Saturation of Hemoglobin With Oxygen at Different Altitudes EFFECT OF BREATHING PURE OXYGEN ON ALVEOLAR Po2 AT DIFFERENT ALTITUDES The “Ceiling” When Breathing Air and When Breathing Oxygen in an Unpressurized Airplane ACUTE EFFECTS OF HYPOXIA Acclimatization to Low Po2 Increased Pulmonary Ventilation—Role of Arterial Chemoreceptors Increase in Red Blood Cells and Hemoglobin Concentration During Acclimatization Increased Diffusing Capacity After Acclimatization Peripheral Circulatory System Changes During Acclimatization—Increased Tissue Capillarity Cellular Acclimatization HYPOXIA-INDUCIBLE FACTORS—A“MASTER SWITCH” FOR THE BODY’S RESPONSE TO HYPOXIA NATURAL ACCLIMATIZATION OF NATIVE PEOPLE LIVING AT HIGH ALTITUDES REDUCED WORK CAPACITY AT HIGH ALTITUDES AND POSITIVE EFFECT OF ACCLIMATIZATION ACUTE MOUNTAIN SICKNESS AND HIGH-ALTITUDE PULMONARY EDEMA CHRONIC MOUNTAIN SICKNESS Bibliography Chapter 45: Physiology of Deep Sea Diving and Other Hyperbaric Conditions Relationship of Pressure to Sea Depth Effect of Sea Depth on the Volume of Gases—Boyle’s Law Effect of High Partial Pressures of Individual Gases on the Body NITROGEN NARCOSIS AT HIGH NITROGEN PRESSURES Oxygen Toxicity at High Pressures Effect of Very High Po2 on Blood Oxygen Transport Effect of High Alveolar Po2 on Tissue Po2 Acute Oxygen Poisoning Excessive Intracellular Oxidation as a Cause of Nervous System Oxygen Toxicity—Oxidizing Free Radicals Chronic Oxygen Poisoning Causes Pulmonary Disability Carbon Dioxide Toxicity at Great Depths in the Sea Decompression of the Diver After Excess Exposure to High Pressure Volume of Nitrogen Dissolved in the Body Fluids at Different Depths Decompression Sickness (Also Known as Bends, Compressed Air Sickness, Caisson Disease, Diver’s Paralysis, Dysbarism) Symptoms of Decompression Sickness (“Bends”) Nitrogen Elimination From the Body; Decompression Tables Tank Decompression and Treatment of Decompression Sickness Self­Contained Underwater Breathing Apparatus (Scuba) Diving Bibliography Unit IX: The Nervous System: A. General Principles and Sensory Physiology Chapter 46: Organization of the Nervous System, Basic Functions of Synapses, and Neurotransmitters GENERAL DESIGN OF THE NERVOUS SYSTEM Central Nervous System Neuron: The Basic Functional Unit SENSORY PART OF THE NERVOUS SYSTEM—SENSORY RECEPTORS MOTOR PART OF THE NERVOUS SYSTEM—EFFECTORS PROCESSING OF INFORMATION—INTEGRATIVE FUNCTION OF THE NERVOUS SYSTEM ROLE OF SYNAPSES IN PROCESSING INFORMATION STORAGE OF INFORMATION—MEMORY Major Levels of Central Nervous System Function Spinal Cord Level Lower Brain or Subcortical Level Higher Brain or Cortical Level Comparison of the Nervous System to A Computer Central Nervous System Synapses TYPES OF SYNAPSES—CHEMICAL AND ELECTRICAL “One­Way” Conduction at Chemical Synapses PHYSIOLOGIC ANATOMY OF THE SYNAPSE Presynaptic Terminals Transmitter Release From Presynaptic Terminals—Role of Calcium Ions Transmitter Actions on Postsynaptic Neurons—Function of Receptor Proteins Ion Channels “Second Messenger” System in the Postsynaptic Neuron Excitatory or Inhibitory Receptors in the Postsynaptic Membrane Excitation Inhibition CHEMICAL SUBSTANCES THAT FUNCTION AS SYNAPTIC TRANSMITTERS Small­Molecule, Rapidly Acting Transmitters Recycling of Small­Molecule Types of Vesicles Characteristics of Some Important Small­Molecule Transmitters Neuropeptides Neuropeptide and Small­Molecule Transmitters May Coexist in the Same Neurons ELECTRICAL EVENTS DURING NEURONAL EXCITATION Resting Membrane Potential of the Neuronal Soma Concentration Differences of Ions Across the Neuronal Somal Membrane Uniform Distribution of Electrical Potential Inside the Neuronal Soma Effect of Synaptic Excitation on the Postsynaptic Membrane—Excitatory Postsynaptic Potential Generation of Action Potentials in the Initial Segment of the Axon Leaving the Neuron—Threshold for Excitation Electrical Events During Neuronal Inhibition Effect of Inhibitory Synapses on the Postsynaptic Membrane—Inhibitory Postsynaptic Potential Presynaptic Inhibition Time Course of Postsynaptic Potentials “Spatial Summation” in Neurons—Threshold for Firing “Temporal Summation” Caused by Successive Discharges of a Presynaptic Terminal Simultaneous Summation of Inhibitory and Excitatory Postsynaptic Potentials Facilitation of Neurons Special Functions of Dendrites for Exciting Neurons Large Spatial Field of Excitation of Dendrites Most Dendrites Cannot Transmit Action Potentials—But They Can Transmit Signals Within the Same Neuron by Electrotonic Conduction Decrement of Electrotonic Conduction in the Dendrites—Greater Excitatory (or Inhibitory) Effect by Synapses Located Near the Soma Summation of Excitation and Inhibition in Dendrites Excitation State of the Neuron and Rate of Firing “Excitatory State” Is the Summated Degree of Excitatory Drive to the Neuron SPECIAL CHARACTERISTICS OF SYNAPTIC TRANSMISSION Fatigue of Synaptic Transmission Effect of Acidosis or Alkalosis on Synaptic Transmission Effect of Hypoxia on Synaptic Transmission Effect of Drugs on Synaptic Transmission Synaptic Delay Bibliography Chapter 47: Sensory Receptors, Neuronal Circuits for Processing Information Types of Sensory Receptors and the Stimuli they Detect Differential Sensitivity of Receptors Modality of Sensation—The “Labeled Line” Principle TRANSDUCTION OF SENSORY STIMULI INTO NERVE IMPULSES Local Electrical Currents at Nerve Endings—Receptor Potentials Mechanisms of Receptor Potentials Maximum Receptor Potential Amplitude Relation of the Receptor Potential to Action Potentials Receptor Potential of the Pacinian Corpuscle—an Example of Receptor Function Relation Between Stimulus Intensity and the Receptor Potential Adaptation of Receptors Mechanisms by Which Receptors Adapt Slowly Adapting Receptors Detect Continuous Stimulus Strength—the “Tonic” Receptors Rapidly Adapting Receptors Detect Change in Stimulus Strength—the “Rate Receptors,” “Movement Receptors,” or “Phasic Receptors.” Predictive Function of the Rate Receptors Signal Intensity Transmission in Nerve Tracts—Spatial and Temporal Summation Spatial Summation Temporal Summation Transmission and Processing of Signals in Neuronal Pools Relaying of Signals Through Neuronal Pools Organization of Neurons for Relaying Signals Threshold and Subthreshold Stimuli—Excitation or Facilitation Inhibition of a Neuronal Pool Divergence of Signals Passing Through Neuronal Pools Convergence of Signals Neuronal Circuit With Both Excitatory and Inhibitory Output Signals PROLONGATION OF A SIGNAL BY A NEURONAL POOL—AFTERDISCHARGE Synaptic Afterdischarge Reverberatory (Oscillatory) Circuit as a Cause of Signal Prolongation Signal Prolongation Characteristics of a Reverberatory Circuit Continuous Signal Output From Some Neuronal Circuits Continuous Discharge Caused by Intrinsic Neuronal Excitability Continuous Signals Emitted From Reverberating Circuits as a Means for Transmitting Information Rhythmical Signal Output Instability and Stability of Neuronal Circuits INHIBITORY CIRCUITS AS A MECHANISM FOR STABILIZING NERVOUS SYSTEM FUNCTION SYNAPTIC FATIGUE AS A MEANS OF STABILIZING THE NERVOUS SYSTEM Automatic Short­Term Adjustment of Pathway Sensitivity by the Fatigue Mechanism Long-Term Changes in Synaptic Sensitivity Caused by Automatic Downregulation or Upregulation of Synaptic Receptors Bibliography Chapter 48: Somatic Sensations: I. General Organization, Tactile and Position Senses Classification of Somatic Senses Other Classifications of Somatic Sensations Detection and Transmission of Tactile Sensations Interrelations Among the Tactile Sensations of Touch, Pressure, and Vibration Tactile Receptors Transmission of Tactile Signals in Peripheral Nerve Fibers Detection of Vibration Detection of Tickle and Itch by Mechanoreceptive Free Nerve Endings Sensory Pathways for Transmitting Somatic Signals Into the Central Nervous System TRANSMISSION IN THE DORSAL COLUMN–MEDIAL LEMNISCAL SYSTEM Anatomy of the Dorsal Column–Medial Lemniscal System Spatial Orientation of the Nerve Fibers in the Dorsal Column–Medial Lemniscal System SOMATOSENSORY CORTEX Somatosensory Areas I and II Spatial Orientation of Signals From Different Parts of the Body in Somatosensory Area I Layers of the Somatosensory Cortex and Their Function The Sensory Cortex Is Organized in Vertical Columns of Neurons; Each Column Detects a Different Sensory Spoton the Body With a Specific Sensory Modality Functions of Somatosensory Area I SOMATOSENSORY ASSOCIATION AREAS Amorphosynthesis Effect of Removing the Somatosensory Association Area Characteristics of Dorsal Column–Medial Lemniscal Signal Transmission and Analysis Basic Neuronal Circuit in the Dorsal Column–Medial Lemniscal System Two­Point Discrimination Effect of Lateral Inhibition to Increase the Degree of Contrast in the Perceived Spatial Pattern Transmission of Rapidly Changing and Repetitive Sensations Vibratory Sensation Position Senses Position Sensory Receptors Processing of Position Sense Information in the Dorsal Column–Medial Lemniscal Pathway Transmission of Sensory Signals in the Anterolateral Pathway CHARACTERISTICS OF TRANSMISSION IN THE ANTEROLATERAL PATHWAY Bibliography Chapter 49: Somatic Sensations: II. Pain, Headache, and Thermal Sensations Fast Pain and Slow Pain and Their Qualities PAIN RECEPTORS AND THEIR STIMULATION Pain Receptors Are Free Nerve Endings Mechanical, Thermal, and Chemical Stimuli Excite Pain Receptors Nonadapting Nature of Pain Receptors Rate of Tissue Damage as a Stimulus for Pain Special Importance of Chemical Pain Stimuli During Tissue Damage Tissue Ischemia as a Cause of Pain Muscle Spasm as a Cause of Pain Dual Pathways for Transmission of Pain Signals Into the Central Nervous System PERIPHERAL PAIN FIBERS—“FAST” AND “SLOW” FIBERS DUAL PAIN PATHWAYS IN THE CORD AND BRAIN STEM—THE NEOSPINOTHALAMIC TRACT AND THE PALEOSPINOTHALAMIC TRACT Neospinothalamic Tract for Fast Pain Termination of the Neospinothalamic Tract in the Brain Stem and Thalamus The Nervous System Can Localize Fast Pain in the Body Glutamate, the Probable Neurotransmitter of the Type Aδ Fast Pain Fibers Paleospinothalamic Pathway for Transmitting Slow­Chronic Pain Substance P, the Probable Slow­Chronic Neurotransmitter of Type C Nerve Endings Projection of Paleospinothalamic Pathway (Slow­Chronic Pain Signals) Into the Brain Stem and Thalamus Poor Capability of the Nervous System to Localize Precisely the Source of Pain Transmitted in the Slow­Chronic Pathway Function of the Reticular Formation, Thalamus, and Cerebral Cortex in the Appreciation of Pain Special Capability of Pain Signals to Arouse Overall Brain Excitability Surgical Interruption of Pain Pathways Pain Suppression (Analgesia) System in the Brain and Spinal Cord The Brain’s Opiate System—Endorphins and Enkephalins Referred Pain Mechanism of Referred Pain Visceral Pain “PARIETAL PAIN” CAUSED BY VISCERAL DISEASE LOCALIZATION OF VISCERAL PAIN—“VISCERAL” AND “PARIETAL” PAIN TRANSMISSION PATHWAYS Localization of Referred Pain Transmitted via Visceral Pathways Parietal Pathway for Transmission of Abdominal and Thoracic Pain Thermal Sensations Thermal Receptors and Their Excitation Stimulation of Thermal Receptors—Sensations of Cold, Cool, Indifferent, Warm, and Hot Stimulatory Effects of Rising and Falling Temperature—Adaptation of Thermal Receptors MECHANISM OF STIMULATION OF THERMAL RECEPTORS Spatial Summation of Thermal Sensations TRANSMISSION OF THERMAL SIGNALS IN THE NERVOUS SYSTEM Bibliography Unit X: The Nervous System: B. The Special Senses Chapter 50: The Eye: I. Optics of Vision Physical Principles of Optics Optics of the Eye Consideration of All Refractive Surfaces of the Eye as a Single Lens—The “Reduced” Eye Formation of an Image on the Retina Mechanism of “accommodation” Accommodation Is Controlled by Parasympathetic Nerves Presbyopia—Loss of Accommodation by the Lens Pupillary Diameter “Depth of Focus” of the Lens System Increases With Decreasing Pupillary Diameter Visual Acuity Clinical Method for Stating Visual Acuity DETERMINATION OF DISTANCE OF AN OBJECT FROM THE EYE—”DEPTH PERCEPTION” Determination of Distance by Sizes of Retinal Images of Known Objects Determination of Distance by Moving Parallax Determination of Distance by Stereopsis—Binocular Vision Fluid System of the Eye—Intraocular Fluid FORMATION OF AQUEOUS HUMOR BY THE CILIARY BODY OUTFLOW OF AQUEOUS HUMOR FROM THE EYE Intraocular Pressure Measuring Intraocular Pressure by Tonometry Bibliography Chapter 51: The Eye: II. Receptor and Neural Function of the Retina Anatomy and Function of the Structural Elements of the Retina The Retina Is Composed of Ten Layers or Boundaries Foveal Region of the Retina and Its Importance in Acute Vision Rods and Cones Are Essential Components of Photoreceptors Pigment Layer of the Retina Photochemistry of Vision Rhodopsin­Retinal Visual Cycle and Excitation of the Rods Rhodopsin and Its Decomposition by Light Energy Re­Formation of Rhodopsin Role of Vitamin A for Formation of Rhodopsin Excitation of the Rod When Rhodopsin Is Activated by Light The Rod Receptor Hyperpolarizes in Response to Light Duration of the Receptor Potential, and Logarithmic Relation of the Receptor Potential to Light Intensity Mechanism Whereby Rhodopsin Decomposition Decreases Membrane Sodium Conductance—The Excitation “Cascade" Photochemistry of Color Vision by the Cones AUTOMATIC REGULATION OF RETINAL SENSITIVITY—LIGHT AND DARK ADAPTATION Value of Light and Dark Adaptation in Vision Color Vision Spectral Sensitivities of the Three Types of Cones Interpretation of Color in the Nervous System Perception of White Light Neural Function of the Retina The Visual Pathway From the Cones to the Ganglion Cells Functions Differently From the Rod Pathway Neurotransmitters Released by Retinal Neurons Transmission of Most Signals Occurs in the Retinal Neurons by Electrotonic Conduction, Not by Action Potentials Lateral Inhibition to Enhance Visual Contrast—Function of the Horizontal Cells Depolarizing and Hyperpolarizing Bipolar Cells Amacrine Cells and Their Functions GANGLION CELLS AND OPTIC NERVE FIBERS Retinal Ganglion Cells and Their Respective Fields W, X, and Y Cells P and M Cells Excitation of the Ganglion Cells Spontaneous, Continuous Action Potentials in the Ganglion Cells Transmission of Changes in Light Intensity—The On-Off Response Transmission of Signals Depicting Contrasts in the Visual Scene—The Role of Lateral Inhibition Transmission of Color Signals by the Ganglion Cells Bibliography Chapter 52: The Eye: III. Central Neurophysiology of Vision Visual Pathways FUNCTION OF THE DORSAL LATERAL GENICULATE NUCLEUS OF THE THALAMUS Organization and Function of the Visual Cortex Primary Visual Cortex Secondary Visual Areas of the Cortex The Primary Visual Cortex has six Major Layers Vertical Neuronal Columns in the Visual Cortex “Color Blobs” in the Visual Cortex Interaction of Visual Signals From the Two Separate Eyes Two Major Pathways for Analysis of Visual Information: (1) The Fast “Position” and “Motion” Pathway and (2) the Accurate Color Pathway Analysis of Contrasts in Visual Images Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells NEURONAL PATTERNS OF STIMULATION DURING ANALYSIS OF VISUAL IMAGES Analysis of Contrasts in Visual Images Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells “Complex” Cells Detect Line Orientation When a Line Is Displaced Laterally or Vertically in the Visual Field Detection of Lines of Specific Lengths, Angles, or Other Shapes DETECTION OF COLOR Eye Movements and Their Control Muscular Control of Eye Movements Neural Pathways for Control of Eye Movements Fixation Movements of the Eyes Mechanism of Involuntary Locking Fixation—Role of the Superior Colliculi Saccadic Movement of the Eyes—A Mechanism of Successive Fixation Points Saccadic Movements During Reading Fixation on Moving Objects—“Pursuit Movement” Superior Colliculi Are Mainly Responsible for Turning the Eyes and Head Toward a Visual Disturbance “FUSION” OF THE VISUAL IMAGES FROM THE TWO EYES Neural Mechanism of Stereopsis for Judging Distances of Visual Objects AUTONOMIC CONTROL OF ACCOMMODATION AND PUPILLARY APERTURE Autonomic Nerves to the Eyes CONTROL OF ACCOMMODATION (FOCUSING THE EYES) Control of Pupillary Diameter Pupillary Light Reflex Bibliography Chapter 53: The Sense of Hearing TYMPANIC MEMBRANE AND THE OSSICULAR SYSTEM CONDUCTION OF SOUND FROM THE TYMPANIC MEMBRANE TO THE COCHLEA “Impedance Matching” by the Ossicular System Attenuation of Sound by Contraction of the Tensor Tympani and Stapedius Muscles TRANSMISSION OF SOUND THROUGH BONE COCHLEA FUNCTIONAL ANATOMY OF THE COCHLEA Basilar Membrane and Resonance in the Cochlea TRANSMISSION OF SOUND WAVES IN THE COCHLEA—“TRAVELING WAVE” Vibration Patterns of the Basilar Membrane for Different Sound Frequencies Vibration Amplitude Pattern of the Basilar Membrane FUNCTION OF THE ORGAN OF CORTI Excitation of the Hair Cells Auditory Signals Are Transmitted Mainly by the Inner Hair Cells Hair Cell Receptor Potentials and Excitation of Auditory Nerve Fibers DETERMINATION OF SOUND FREQUENCY—THE “PLACE” PRINCIPLE DETERMINATION OF LOUDNESS Detection of Changes in Loudness—The Power Law Decibel Unit Threshold for Hearing Sound at Different Frequencies Frequency Range of Hearing CENTRAL AUDITORY MECHANISMS AUDITORY NERVOUS PATHWAYS FUNCTION OF THE CEREBRAL CORTEX IN HEARING Sound Frequency Perception in the Primary Auditory Cortex Discrimination of Sound “Patterns” by the Auditory Cortex DETERMINATION OF THE DIRECTION FROM WHICH SOUND COMES Neural Mechanisms for Detecting Sound Direction Bibliography Chapter 54: The Chemical Senses—Taste and Smell Sense of Taste Primary Taste Sensations Sour Taste Salty Taste Sweet Taste Bitter Taste Umami Taste Threshold for Taste Taste Blindness Taste Buds and Their Function Location of the Taste Buds Specificity of Taste Buds for a Primary Taste Stimulus Mechanism of Stimulation of Taste Buds Receptor Potential Generation of Nerve Impulses by the Taste Bud TRANSMISSION OF TASTE SIGNALS INTO THE CENTRAL NERVOUS SYSTEM Taste Reflexes Are Integrated in the Brain Stem Rapid Adaptation of Taste TASTE PREFERENCE AND CONTROL OF THE DIET Sense of Smell Olfactory Membrane Olfactory Cells Are the Receptor Cells for Smell Sensation Stimulation of the Olfactory Cells Mechanism of Excitation of the Olfactory Cells Membrane Potentials and Action Potentials in Olfactory Cells Rapid Adaptation of Olfactory Sensations Search for the Primary Sensations of Smell Affective Nature of Smell Threshold for Smell Gradations of Smell Intensities TRANSMISSION OF SMELL SIGNALS INTO THE CENTRAL NERVOUS SYSTEM Transmission of Olfactory Signals Into the Olfactory Bulb Primitive and Newer Olfactory Pathways Into the Central Nervous System The Primitive Olfactory System—The Medial Olfactory Area The Less Old Olfactory System—The Lateral Olfactory Area The Newer Pathway Summary Centrifugal Control of Activity in the Olfactory Bulb by the Central Nervous System Bibliography Unit XI: The Nervous System: C. Motor and Integrative Neurophysiology Chapter 55: Spinal Cord Motor Functions; the Cord Reflexes Organization of the Spinal Cord for Motor Functions Anterior Motor Neurons Alpha Motor Neurons Gamma Motor Neurons Interneurons Muscle Sensory Receptors—Muscle Spindles and Golgi Tendon Organs—and Their Roles in Muscle Control Receptor Function of the Muscle Spindle Structure and Motor Innervation of the Muscle Spindle Sensory Innervation of the Muscle Spindle Primary Ending Secondary Ending Division of the Intrafusal Fibers Into Nuclear Bag and Nuclear Chain Fibers—Dynamic and Static Responses of the Muscle Spindle The Primary and the Secondary Endings Both Respond to the Length of the Receptor—“Static” Response The Primary Ending (but Not the Secondary Ending) Responds to Rate of Change of Receptor Length—“Dynamic” Response Control of Intensity of the Static and Dynamic Responses by the Gamma Motor Nerves Continuous Discharge of the Muscle Spindles Under Normal Conditions Muscle Stretch Reflex Neuronal Circuitry of the Stretch Reflex Dynamic Stretch Reflex and Static Stretch Reflexes “Damping” Function of the Dynamic and Static Stretch Reflexes in Smoothing Muscle Contraction ROLE OF THE MUSCLE SPINDLE IN VOLUNTARY MOTOR ACTIVITY Brain Areas for Control of the Gamma Motor System The Muscle Spindle System Stabilizes Body Position During Tense Action Golgi Tendon Reflex Golgi Tendon Organ Helps Control Muscle Tension Transmission of Impulses From the Tendon Organ Into the Central Nervous System The Tendon Reflex Prevents Excessive Tension on the Muscle Possible Role of the Tendon Reflex to Equalize Contractile Force Among the Muscle Fibers Function of the Muscle Spindles and Golgi Tendon Organs in Motor Control by Higher Levels of the Brain Flexor Reflex and the Withdrawal Reflexes Neuronal Mechanism of the Flexor Reflex Pattern of Withdrawal During Flexor Reflex Crossed Extensor Reflex Neuronal Mechanism of the Crossed Extensor Reflex Reciprocal Inhibition and Reciprocal Innervation REFLEXES OF POSTURE AND LOCOMOTION Postural and Locomotive Reflexes of the Cord Positive Supportive Reaction Cord “Righting” Reflexes Stepping and Walking Movements Rhythmical Stepping Movements of a Single Limb Reciprocal Stepping of Opposite Limbs Diagonal Stepping of All Four Limbs—“Mark Time” Reflex Bibliography Chapter 56: Cortical and Brain Stem Control of Motor Function Motor Cortex and Corticospinal Tract Primary Motor Cortex Premotor Area Supplementary Motor Area SOME SPECIALIZED AREAS OF MOTOR CONTROL FOUND IN THE HUMAN MOTOR CORTEX Broca’s Area (Motor Speech Area) “Voluntary” Eye Movement Field Head Rotation Area Area for Hand Skills TRANSMISSION OF SIGNALS FROM THE MOTOR CORTEX TO THE MUSCLES Corticospinal (Pyramidal) Tract THE RED NUCLEUS SERVES AS AN ALTERNATIVE PATHWAY FOR TRANSMITTING CORTICAL SIGNALS TO THE SPINAL CORD The Corticorubrospinal System Is an Accessory Pathway for Transmitting Relatively Discrete Signals From the Motor Cortex to the Spinal Cord EXCITATION OF THE SPINAL CORD MOTOR CONTROL AREAS BY THE PRIMARY MOTOR CORTEX AND RED NUCLEUS Neurons in the Motor Cortex Are Arranged in Vertical Columns Each Column of Neurons Functions as an Integrative Processing System Dynamic and Static Signals Are Transmitted by the Pyramidal Neurons Somatosensory Feedback to the Motor Cortex Helps Control Precision of Muscle Contraction Stimulation of the Spinal Motor Neurons Patterns of Movement Elicited by Spinal Cord Centers Control of Motor Functions by the Brain Stem SUPPORT OF THE BODY AGAINST GRAVITY—ROLES OF THE RETICULAR AND VESTIBULAR NUCLEI Excitatory­Inhibitory Antagonism Between Pontine and Medullary Reticular Nuclei Pontine Reticular System Transmits Excitatory Signals Medullary Reticular System Transmit Inhibitory Signals Role of the Vestibular Nuclei to Excite the Antigravity Muscles The Decerebrate Animal Develops Spastic Rigidity VESTIBULAR SENSATIONS AND MAINTENANCE OF EQUILIBRIUM Vestibular Apparatus “Maculae”—Sensory Organs of the Utricle and Saccule for Detecting Orientation of the Head With Respect to Gravity Directional Sensitivity of the Hair Cells—Kinocilium Semicircular Ducts Function of the Utricle and Saccule in the Maintenance of Static Equilibrium Detection of Linear Acceleration by the Utricle and Saccule Maculae Detection of Head Rotation by the Semicircular Ducts “Predictive” Function of the Semicircular Duct System in the Maintenance of Equilibrium Bibliography Chapter 57: Cerebellum and Basal Ganglia Contributions to Overall Motor Control The Cerebellum and its Motor Functions FUNCTIONAL UNIT OF THE CEREBELLAR CORTEX—THE PURKINJE AND DEEP NUCLEAR CELLS Neuronal Circuit of the Functional Unit Purkinje Cells and Deep Nuclear Cells Fire Continuously Under Normal Resting Conditions Balance Between Excitation and Inhibition at the Deep Cerebellar Nuclei Basket Cells and Stellate Cells Cause Lateral Inhibition of Purkinje Cells in the Cerebellum Turn­On/Turn-Off and Turn­Off/Turn­On Output Signals From the Cerebellum The Purkinje Cells “Learn” to Correct Motor Errors—Role of the Climbing Fibers FUNCTION OF THE CEREBELLUM IN OVERALL MOTOR CONTROL The Vestibulocerebellum Functions in Association With the Brain Stem and Spinal Cord to Control Equilibrium and Postural Movements Spinocerebellum—Feedback Control of Distal Limb Movements via the Intermediate Cerebellar Cortex and the Interposed Nucleus Function of the Cerebellum to Prevent Overshoot and to “Damp” Movements Cerebellar Control of Ballistic Movements Cerebrocerebellum—Function of the Large Lateral Zone of the Cerebellar Hemisphere to Plan, Sequence, and Time Complex Movements Planning of Sequential Movements Timing Function for Sequential Movements Extramotor Predictive Functions of the Cerebrocerebellum The Basal Ganglia and Their Motor Functions NEURONAL CIRCUITRY OF THE BASAL GANGLIA FUNCTION OF THE BASAL GANGLIA IN EXECUTING PATTERNS OF MOTOR ACTIVITY—THE PUTAMEN CIRCUIT Neural Pathways of the Putamen Circuit Abnormal Function in the Putamen Circuit: Athetosis, Hemiballismus, and Chorea ROLE OF THE BASAL GANGLIA FOR COGNITIVE CONTROL OF MOTOR PATTERN SEQUENCES—THE CAUDATE CIRCUIT FUNCTION OF THE BASAL GANGLIA TO CHANGE THE TIMING AND TO SCALE THE INTENSITY OF MOVEMENTS FUNCTIONS OF SPECIFIC NEUROTRANSMITTER SUBSTANCES IN THE BASAL GANGLIAL SYSTEM Integration of the Many Parts of the Total Motor Control System Spinal Level Hindbrain Level Motor Cortex Level Associated Functions of the Cerebellum Associated Functions of the Basal Ganglia What drives us to action Bibliography Chapter 58: Cerebral Cortex, Intellectual Functions of the Brain, Learning, and Memory Physiologic Anatomy of the Cerebral Cortex ANATOMICAL AND FUNCTIONAL RELATIONS OF THE CEREBRAL CORTEX TO THE THALAMUS AND OTHER LOWER CENTERS Functions of Specific Cortical Areas Association Areas Parieto­Occipitotemporal Association Area Analysis of the Spatial Coordinates of the Body Wernicke’s Area Is Important for Language Comprehension The Angular Gyrus Area Is Needed for Initial Processing of Visual Language (Reading) Area for Naming Objects Prefrontal Association Area Broca’s Area Provides the Neural Circuitry for Word Formation. Broca’s area, shown in Figure 58-­5, is located partly in the pos... Limbic Association Area Area for Recognition of Faces COMPREHENSIVE INTERPRETATIVE FUNCTION OF THE POSTERIOR SUPERIOR TEMPORAL LOBE—”WERNICKE’S AREA” (A GENERAL INTERPRETATIVE AREA) Angular Gyrus—Interpretation of Visual Information Concept of the Dominant Hemisphere Role of Language in the Function of Wernicke’s Area and in Intellectual Functions FUNCTIONS OF THE PARIETO-OCCIPITOTEMPORAL CORTEX IN THE NONDOMINANT HEMISPHERE HIGHER INTELLECTUAL (“EXECUTIVE”) FUNCTIONS OF THE PREFRONTAL ASSOCIATION AREAS Decreased Aggressiveness and Inappropriate Social Responses Inability to Progress Toward Goals or to Carry Through Sequential Thoughts Elaboration of Thought, Prognostication, and Performance of Higher Intellectual Functions by the Prefrontal Areas—Concept of a “Working Memory" THE CORPUS CALLOSUM AND ANTERIOR COMMISSURE TRANSFER THOUGHTS, MEMORIES, TRAINING, AND OTHER INFORMATION BETWEEN THE TWO CEREBRAL HEMISPHERES Thoughts, Consciousness, and Memory MEMORY—ROLES OF SYNAPTIC FACILITATION AND SYNAPTIC INHIBITION Positive and Negative Memory—“Sensitization” or “Habituation” of Synaptic Transmission Classification of Memories Short­Term Memory Intermediate Long­Term Memory Memory Based on Chemical Changes in Presynaptic Terminals or Postsynaptic Neuronal Membranes Molecular Mechanism of Intermediate Memory Mechanism for Habituation Mechanism for Facilitation Long­Term Memory Structural Changes Occur in Synapses During Development of Long­Term Memory Number of Neurons and Their Connectivities Often Change Significantly During Learning Consolidation of Memory Rehearsal Enhances the Transference of Short­Term Memory Into Long­Term Memory New Memories Are Codified During Consolidation Role of the Hippocampus and Other Brain Regions in Memory Anterograde Amnesia—Inability to Create New Declarative Long-Term Memories After Hippocampal Lesions Retrograde Amnesia—Inability to Recall Memories From the Past After Hippocampal or Thalmic Lesions Hippocampi Are Not Important in Reflexive Learning Bibliography Chapter 59: The Limbic System and the Hypothalamus—Behavioral and Motivational Mechanisms of the Brain Activating—Driving Systems Of The Brain Control Of Cerebral Activity By Continuous Excitatory Signals From The Brain Stem Reticular Excitatory Area of the Brain Stem—a Driver of Brain Activity Excitation of the Reticular Excitatory Area by Peripheral Sensory Signals Increased Activity of the Excitatory Area Causedby Feedback Signals Returning From the Cerebral Cortex The Thalamus Is a Distribution Center That Controls Activity in Specific Regions of the Cortex A Reticular Inhibitory Area Is Located in the Lower Brain Stem NEUROHORMONAL CONTROL OF BRAIN ACTIVITY Neurohormonal Systems in the Human Brain Other Neurotransmitters and Neurohormonal Substances Secreted in the Brain Limbic System FUNCTIONAL ANATOMY OF THE LIMBIC SYSTEM—KEY POSITION OF THE HYPOTHALAMUS The Hypothalamus, a Major Control Headquarters for the Limbic System VEGETATIVE AND ENDOCRINE CONTROL FUNCTIONS OF THE HYPOTHALAMUS Cardiovascular Regulation Body Temperature Regulation Body Water Regulation Regulation of Uterine Contractility and Milk Ejection from the Breasts Gastrointestinal and Feeding Regulation Hypothalamic Control of Endocrine Hormone Secretion by the Anterior Pituitary Gland Hypothalamic Control of Circadian Rhythms—The Suprachiasmatic Nucleus Summary Behavioral Functions of the Hypothalamus and Associated Limbic Structures Effects Caused by Stimulation of the Hypothalamus Effects Caused by Hypothalamic Lesions “REWARD” AND “PUNISHMENT” FUNCTION OF THE LIMBIC SYSTEM Reward Centers Punishment Centers Association of Rage With Punishment Centers Placidity and Tameness IMPORTANCE OF REWARD OR PUNISHMENT ON BEHAVIOR Effect of Tranquilizers on the Reward or Punishment Centers Importance of Reward or Punishment in Learning and Memory—Habituation Versus Reinforcement SPECIFIC FUNCTIONS OF OTHER PARTS OF THE LIMBIC SYSTEM Functions Of The Hippocampus Role of the Hippocampus in Learning Anterograde Amnesia After Bilateral Removal of the Hippocampi Theoretical Function of the Hippocampus in Learning Bibliography Chapter 60: States of Brain Activity—Sleep, Brain Waves, Epilepsy, Psychoses, and Dementia Sleep TWO TYPES OF SLEEP—SLOW-WAVE SLEEP AND RAPID EYE MOVEMENT SLEEP REM (Paradoxical, Desynchronized) Sleep Slow­Wave Sleep Basic Theories of Sleep Sleep Is Caused by an Active Inhibitory Process Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep—Possible Role for Serotonin Lesions in Sleep­Promoting Centers Can Cause Intense Wakefulness Other Possible Transmitter Substances Related to Sleep Possible Cause of REM Sleep Cycle Between Sleep and Wakefulness SLEEP HAS IMPORTANT PHYSIOLOGICAL FUNCTIONS Bibliography Chapter 61: The Autonomic Nervous System and the Adrenal Medulla General Organization of the Autonomic Nervous System BASIC CHARACTERISTICS OFS YMPATHETIC AND PARASYMPATHETIC FUNCTION Cholinergic and Adrenergic Fibers—Secretion of Acetylcholine or Norepinephrine Mechanisms of Transmitter Secretion and Removal at Postganglionic Endings Secretion of Acetylcholine and Norepinephrine by Postganglionic Nerve Endings Synthesis of Acetylcholine, Its Destruction After Secretion, and Its Duration of Action Synthesis of Norepinephrine, Its Removal, and Its Duration of Action Receptors on the Effector Organs Excitation or Inhibition of the Effector Cell by Changing Its Membrane Permeability Receptor Action by Altering Intracellular “Second Messenger” Enzymes Two Principal Types of Acetylcholine Receptors—Muscarinic and Nicotinic Receptors Alpha and Beta Adrenergic Receptors Function of the Adrenal Medullae The Adrenal Medullae Support Sympathetic Nervous System Functions. Epinephrine and norepinephrine are almost always released by ... Tone Caused by Basal Secretion of Epinephrine and Norepinephrine by the Adrenal Medullae. The normal resting rate of secretion b... Effect of Loss of Sympathetic or Parasympathetic Tone After Denervation. Immediately after a sympathetic or parasympathetic nerv... EXCITATORY AND INHIBITORY ACTIONS OF SYMPATHETIC AND PARASYMPATHETIC STIMULATION FUNCTION OF THE ADRENAL MEDULLAE The Adrenal Medullae Support Sympathetic Nervous System Functions RELATION OF STIMULUS RATE TO SYMPATHETIC AND PARASYMPATHETIC EFFECTS SYMPATHETIC AND PARASYMPATHETIC “TONE” Tone Caused by Basal Secretion of Epinephrine and Norepinephrine by the Adrenal Medullae Effect of Loss of Sympathetic or Parasympathetic Tone After Denervation Selective Stimulation of Target Organs by Sympathetic and Parasympathetic Systems or “Mass Discharge” The Sympathetic System Sometimes Responds by Mass Discharge The Parasympathetic System Usually Causes Specific Localized Responses “ALARM” OR “STRESS” RESPONSE OF THE SYMPATHETIC NERVOUS SYSTEM MEDULLARY, PONTINE, AND MESENCEPHALIC CONTROL OF THE AUTONOMIC NERVOUS SYSTEM Control of Brain Stem Autonomic Centers by Higher Areas Bibliography Chapter 62: Cerebral Blood Flow, Cerebrospinal Fluid, and Brain Metabolism Cerebral Blood Flow Regulation of Cerebral Blood Flow Excesses of CO2 or H+ Concentration Increase Cerebral Blood Flow Importance of Cerebral Blood Flow Control by CO2 and H+ Oxygen Deficiency as a Regulator of Cerebral Blood Flow Cerebral Microcirculation Cerebrospinal Fluid System CUSHIONING FUNCTION OF THE CEREBROSPINAL FLUID FORMATION, FLOW, AND ABSORPTION OF CEREBROSPINAL FLUID Secretion by the Choroid Plexus Absorption of Cerebrospinal Fluid Through the Arachnoidal Villi Perivascular Spaces and Cerebrospinal Fluid Lymphatic Function of the Perivascular Spaces Brain Metabolism Total Brain Metabolic Rate and Metabolic Rate of Neurons Special Requirement of the Brain for Oxygen—Lack of Significant Anaerobic Metabolism Under Normal Conditions, Most Brain Energy Is Supplied by Glucose Bibliography Unit XII: Gastrointestinal Physiology Chapter 63: General Principles of Gastrointestinal Function—Motility, Nervous Control, and Blood Circulation GENERAL PRINCIPLES OF GASTROINTESTINAL MOTILITY Physiologic Anatomy of the Gastrointestinal Wall Gastrointestinal Smooth Muscle Functions as a Syncytium Electrical Activity of Gastrointestinal Smooth Muscle “Slow Waves” Caused by Undulating Changes in Resting Membrane Potential Spike Potentials Changes in Voltage of the Resting Membrane Potential Entry of Calcium Ions Causes Smooth Muscle Contraction Tonic Contraction of Some Gastrointestinal Smooth Muscle Neural Control of Gastrointestinal Function—Enteric Nervous System DIFFERENCES BETWEEN THE MYENTERIC AND SUBMUCOSAL PLEXUSES TYPES OF NEUROTRANSMITTERS SECRETED BY ENTERIC NEURONS Autonomic Control of the Gastrointestinal Tract Parasympathetic Stimulation Increases Activity of the Enteric Nervous System Sympathetic Stimulation Usually Inhibits Gastrointestinal Tract Activity Afferent Sensory Nerve Fibers From the Gut Gastrointestinal Reflexes Hormonal Control of Gastrointestinal Motility Functional Movements in the Gastrointestinal Tract PROPULSIVE MOVEMENTS—PERISTALSIS Function of the Myenteric Plexus in Peristalsis Peristaltic Waves Move Toward the Anus With Downstream Receptive Relaxation—“Law of the Gut” SEGMENTATION CONTRACTIONS—MIXING MOVEMENTS Gastrointestinal Blood Flow—Splanchnic Circulation ANATOMY OF THE GASTROINTESTINAL BLOOD SUPPLY EFFECT OF GUT ACTIVITY AND METABOLIC FACTORS ON GASTROINTESTINAL BLOOD FLOW Mechanisms of Increased Blood Flow During Gastrointestinal Activity “Countercurrent” Blood Flow in the Villi NERVOUS CONTROL OF GASTROINTESTINAL BLOOD FLOW Importance of Nervous Depression of Gastrointestinal Blood Flow When Other Parts of the Body Need Extra Blood Flow Bibliography Chapter 64: Propulsion and Mixing of Food in the Alimentary Tract Ingestion of Food Mastication (Chewing) Swallowing (Deglutition) Voluntary Stage of Swallowing Involuntary Pharyngeal Stage of Swallowing Nervous Initiation of the Pharyngeal Stage of Swallowing The Pharyngeal Stage of Swallowing Momentarily Interrupts Respiration The Esophageal Stage of Swallowing Involves Two Types of Peristalsis Receptive Relaxation of the Stomach Function of the Lower Esophageal Sphincter (Gastroesophageal Sphincter) Prevention of Esophageal Reflux by Valvelike Closure of the Distal End of the Esophagus Motor Functions of the Stomach Storage Function of the Stomach FOOD MIXING AND PROPULSION IN THE STOMACH—BASIC ELECTRICAL RHYTHM OF THE STOMACH WALL Chyme Hunger Contractions Stomach Emptying Intense Antral Peristaltic Contractions During Stomach Emptying—“Pyloric Pump” Role of the Pylorus in Controlling Stomach Emptying Regulation of Stomach Emptying Gastric Factors That Promote Emptying Effect of Gastric Food Volume on Rate of Emptying The Hormone Gastrin Promotes Stomach Emptying Powerful Duodenal Factors That Inhibit Stomach Emptying Duodenum Enterogastric Nervous Reflexes Inhibit Stomach Emptying Hormonal Feedback From the Duodenum Inhibits Gastric Emptying—Role of Fats and the Hormone Cholecystokinin Summary of the Control of Stomach Emptying Movements of the Small Intestine MIXING CONTRACTIONS (SEGMENTATION CONTRACTIONS) Propulsive Movements Peristalsis in the Small Intestine Control of Peristalsis by Nervous and Hormonal Signals Propulsive Effect of the Segmentation Movements Powerful, Rapid Peristalsis—“Peristaltic Rush” THE ILEOCECAL VALVE PREVENTS BACKFLOW FROM THE COLON TO THE SMALL INTESTINE Feedback Control of the Ileocecal Sphincter by Reflexes From the Cecum Movements of the Colon Mixing Movements—“Haustrations” Propulsive Movements—“Mass Movements” Initiation of Mass Movements by Gastrocolic and Duodenocolic Reflexes Defecation Defecation Reflexes Other Autonomic Reflexes That Affect Bowel Activity Bibliography Chapter 65: Secretory Functions of the Alimentary Tract GENERAL PRINCIPLES OF ALIMENTARY TRACT SECRETION TYPES OF ALIMENTARY TRACT GLANDS Basic Mechanisms of Stimulation of the Alimentary Tract Glands Contact of Food With Gut Epithelium Activates the Enteric Nervous System and Stimulates Secretion Autonomic Stimulation of Secretion Parasympathetic Stimulation Increases Alimentary Tract Glandular Secretion Rate Sympathetic Stimulation Has a Dual Effect on Alimentary Tract Glandular Secretion Rate Regulation of Glandular Secretion by Hormones Basic Mechanism of Secretion by Glandular Cells Secretion of Organic Substances Water and Electrolyte Secretion Secretion of Saliva Saliva Contains a Serous Secretion and a Mucus Secretion Secretion of Ions in Saliva NERVOUS REGULATION OF SALIVARY SECRETION Gastric Secretion Secretions From the Gastric (Oxyntic) Glands Basic Mechanism of Hydrochloric Acid Secretion The Basic Factors That Stimulate Gastric Secretion Are Acetylcholine, Gastrin, and Histamine Secretion and Activation of Pepsinogen Secretion of Intrinsic Factor by Parietal Cells PYLORIC GLANDS SECRETE MUCUS AND GASTRIN Surface Mucous Cells Stimulation of Gastric Acid Secretion Parietal Cells of the Oxyntic Glands Are the Only Cells That Secrete Hydrochloric Acid Stimulation of Acid Secretion by Gastrin Regulation of Pepsinogen Secretion Pancreatic Secretion Pancreatic Digestive Enzymes Secretion of Trypsin Inhibit or Prevents Digestion of the Pancreas Secretion of Bicarbonate Ions Regulation of Pancreatic Secretion Basic Stimuli That Cause Pancreatic Secretion Multiplicative Effects of Different Stimuli Phases of Pancreatic Secretion Cephalic and Gastric Phases Intestinal Phase Secretin Stimulates Copious Secretion of Bicarbonate Ions, Which Neutralizes Acidic Stomach Chyme Cholecystokinin Contributes to Control of Digestive Enzyme Secretion by the Pancreas Bile Secretion by the Liver PHYSIOLOGIC ANATOMY OF BILIARY SECRETION The Gallbladder Stores and Concentrates Bile Composition of Bile Cholecystokinin Stimulates Gallbladder Emptying FUNCTION OF BILE SALTS IN FAT DIGESTION AND ABSORPTION Secretions of the Small Intestine Secretion of Mucus by Brunner's Glands in the Duodenum SECRETION OF INTESTINAL DIGESTIVEJUICES BY THE CRYPTS OF LIEBERKÜHN Mechanism of Secretion of the Watery Fluid Digestive Enzymes in the Small Intestinal Secretion REGULATION OF SMALL INTESTINE SECRETION—LOCAL STIMULI Secretion of Mucus by The Large Intestine Mucus Secretion Diarrhea Caused by Excess Secretion of Water and Electrolytes in Response to Irritation Bibliography Chapter 66: Digestion and Absorption in the Gastrointestinal Tract DIGESTION OF VARIOUS FOODS BY HYDROLYSIS Hydrolysis of Carbohydrates Hydrolysis of Fats Hydrolysis of Proteins Digestion of Carbohydrates Carbohydrate Foods of the Diet Digestion of Carbohydrates Begins in the Mouth and Stomach Digestion of Carbohydrates in the Small Intestine Digestion by Pancreatic Amylase Hydrolysis of Disaccharides and Small Glucose Polymers Into Monosaccharides by Intestinal Epithelial Enzymes Digestion of Proteins Proteins of the Diet Digestion of Proteins in the Stomach Most Protein Digestion Results From Actions of Pancreatic Proteolytic Enzymes Digestion of Peptides by Peptidases in the Enterocytes That Line the Small Intestinal Villi Digestion of Fats Fats of the Diet Digestion of Fats Occurs Mainly in the Small Intestine The First Step in Fat Digestion Is Emulsification by Bile Acids and Lecithin Triglycerides Are Digested by Pancreatic Lipase End Products of Fat Digestion Are Free Fatty Acids Bile Salts Form Micelles That Accelerate Fat Digestion Digestion of Cholesterol Esters and Phospholipids Basic Principles of Gastrointestinal Absorption Anatomical Basis of Absorption Folds of Kerckring, Villi, and Microvilli Increase the Mucosal Absorptive Area by Nearly 1000-Fold Absorption in the Small Intestine Isosmotic Absorption of Water Absorption of Ions Sodium Is Actively Transported Through the Intestinal Membrane Osmosis of the Water Aldosterone Greatly Enhances Sodium Absorption Absorption of Chloride Ions in the Small Intestine Absorption of Bicarbonate Ions in the Duodenum and Jejunum Secretion of Bicarbonate and Absorption of Chloride Ions in the Ileum and Large Intestine Active Absorption of Calcium, Iron, Potassium, Magnesium, and Phosphate Absorption of Nutrients Carbohydrates Are Mainly Absorbed as Monosaccharides Glucose Is Transported by a Sodium Co­Transport Mechanism Absorption of Other Monosaccharides Absorption of Proteins as Dipeptides, Tripeptides, or Amino Acids Absorption of Fats Direct Absorption of Fatty Acids Into the Portal Blood Absorption in the Large Intestine: Formation of Feces Absorption and Secretion of Electrolytes and Water Maximum Absorption Capacity of the Large Intestine Composition of the Feces Bibliography Chapter 67: Physiology of Gastrointestinal Disorders Bibliography Unit XIII: Metabolism and Temperature Regulation Chapter 68: Metabolism of Carbohydrates and Formation of Adenosine Triphosphate Bibliography Chapter 69: Lipid Metabolism Basic Chemical Structure of Triglycerides (Neutral Fat) TRANSPORT OF LIPIDS IN THE BODY FLUIDS Transport of Triglycerides and Other Lipids From the Gastrointestinal Tract by Lymph—the Chylomicrons REMOVAL OF THE CHYLOMICRONS FROM THE BLOOD Chylomicron Triglycerides Are Hydrolyzed by Lipoprotein Lipase, and Fat Is Stored in Adipose Tissue Bibliography Chapter 70: Protein Metabolism Bibliography Chapter 71: The Liver Bibliography Chapter 72: Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and Minerals ENERGY INTAKE AND OUTPUT BALANCED UNDER STEADY­STATE CONDITIONS REGULATION OF FOOD INTAKE AND ENERGY STORAGE NEURAL CENTERS REGULATE FOOD INTAKE The Hypothalamus Contains Hunger and Satiety Centers Neurons and Neurotransmitters in the Hypothalamus That Stimulate or Inhibit Feeding Neural Centers That Influence the Mechanical Process of Feeding FACTORS THAT REGULATE QUANTITY OF FOOD INTAKE Short­Term Regulation of Food Intake Gastrointestinal Filling Inhibits Feeding Gastrointestinal Hormonal Factors Suppress Feeding Ghrelin, a Gastrointestinal Hormone, Increases Feeding Oral Receptors Meter Food Intake Intermediate­ and Long­Term Regulation of Food Intake Effect of Blood Concentrations of Glucose, Amino Acids, and Lipids on Hunger and Feeding Temperature Regulation and Food Intake Feedback Signals From Adipose Tissue Regulate Food Intake Summary of Long-Term Regulation Importance of Having Both Long­ and Short­Term Regulatory Systems for Feeding Bibliography Chapter 73: Energetics and Metabolic Rate Bibliography Chapter 74: Body Temperature Regulation and Fever Normal Body Temperatures Body Core Temperature and Skin Temperature Normal Core Temperature Body Temperature is Controlled by Balancing Heat Production and Heat Loss Heat Production Heat Loss Insulator System of the Body Blood Flow to the Skin From the Body Core Provides Heat Transfer Control of Heat Conduction to the Skin by the Sympathetic Nervous System Basic Physics of Heat Loss From the Skin Surface Radiation Causes Heat Loss in the Form of Infrared Rays Conductive Heat Loss Occurs by Direct Contact With an Object Convective Heat Loss Results From Air Movement Cooling Effect of Wind Conduction and Convection of Heat From a Person Suspended in Water Evaporation Evaporation is a Necessary Cooling Mechanism at Very High Air Temperatures Clothing Reduces Conductive and Convective Heat Loss Sweating and Its Regulation by the Autonomic Nervous System Mechanism of Sweat Secretion Acclimatization of the Sweating Mechanism to Heat—The Role of Aldosterone Regulation of Body Temperature—Role of the Hypothalamus ROLE OF THE ANTERIOR HYPOTHALAMIC-PREOPTIC AREA IN THERMOSTATIC DETECTION OF TEMPERATURE DETECTION OF TEMPERATURE BY RECEPTORS IN THE SKIN AND DEEP BODY TISSUES POSTERIOR HYPOTHALAMUS INTEGRATES CENTRAL AND PERIPHERAL TEMPERATURE SENSORY SIGNALS NEURONAL EFFECTOR MECHANISMS THAT DECREASE OR INCREASE BODY TEMPERATURE Temperature­Decreasing Mechanisms When the Body Is Too Hot Temperature­Increasing Mechanisms When the Body Is Too Cold Hypothalamic Stimulation of Shivering Sympathetic “Chemical” Excitation of Heat Production Increased Thyroxine Output as a Long­Term Cause of Increased Heat Production “SET POINT” FOR TEMPERATURE CONTROL Feedback Gain for Body Temperature Control Skin Temperature Can Slightly Alter the Set Point for Core Temperature Control BEHAVIORAL CONTROL OF BODY TEMPERATURE ABNORMALITIES OF BODY TEMPERATURE REGULATION Fever Resetting the Hypothalamic Temperature­Regulating Center in Febrile Diseases—Effect of Pyrogens Mechanism of Action of Pyrogens in Causing Fever—Role of Cytokines Fever Caused by Brain Lesions Bibliography Unit XIV: Endocrinology and Reproduction Chapter 75: Introduction to Endocrinology Coordination of Body Functions by Chemical Messengers Chemical Structure and Synthesis of Hormones Polypeptide and Protein Hormones Are Stored in Secretory Vesicles Until Needed Steroid Hormones Are Usually Synthesized From Cholesterol and Are Not Stored Amine Hormones Are Derived From Tyrosine HORMONE SECRETION, TRANSPORT, AND CLEARANCE FROM THE BLOOD Hormone Secretion After a Stimulus and Duration of Action of Different Hormones Concentrations of Hormones in the Circulating Blood and Hormonal Secretion Rates Feedback Control of Hormone Secretion Negative Feedback Prevents Overactivity of Hormone Systems Surges of Hormones Can Occur With Positive Feedback Cyclical Variations Occur in Hormone Release TRANSPORT OF HORMONES IN THE BLOOD “Clearance” of Hormones From the Blood MECHANISMS OF ACTION OF HORMONES Hormone Receptors and their Activation The Number and Sensitivity of Hormone Receptors Are Regulated INTRACELLULAR SIGNALING AFTER HORMONE RECEPTOR ACTIVATION Ion Channel–Linked Receptors G Protein–Linked Hormone Receptors Enzyme-­Linked Hormone Receptors Intracellular Hormone Receptors and Activation of Genes SECOND MESSENGER MECHANISMS FOR MEDIATING INTRACELLULAR HORMONAL FUNCTIONS Adenylyl Cyclase–cAMP Second Messenger System Cell Membrane Phospholipid Second Messenger System Calcium-­Calmodulin Second Messenger System Hormones that Act Mainly on the Genetic Machinery of the Cell Steroid Hormones Increase Protein Synthesis Thyroid Hormones Increase Gene Transcription in the Cell Nucleus Bibliography Chapter 76: Pituitary Hormones and Their Control by the Hypothalamus PITUITARY GLAND AND ITS RELATION TO THE HYPOTHALAMUS ANTERIOR AND POSTERIOR LOBES OF THE PITUITARY GLAND Posterior Pituitary Hormones Are Synthesized by Cell Bodies in the Hypothalamus Hypothalamus Controls Pituitary Secretion HYPOTHALAMIC-HYPOPHYSIAL PORTAL BLOOD VESSELS OF THE ANTERIOR PITUITARY GLAND Hypothalamic Releasing and Inhibitory Hormones Are Secreted Into the Median Eminence Hypothalamic Releasing and Inhibitory Hormones Control Anterior Pituitary Secretion Specific Areas in the Hypothalamus Control Secretion of Specific Hypothalamic Releasing and Inhibitory Hormones Physiological Functions of Growth Hormone GROWTH HORMONE PROMOTES GROWTH OF MANY BODY TISSUES GROWTH HORMONE HAS SEVERAL METABOLIC EFFECTS Growth Hormone Promotes Protein Deposition in Tissues Enhancement of Amino Acid Transport Through the Cell Membranes Enhancement of RNA Translation to Cause Protein Synthesis by the Ribosomes Increased Nuclear Transcription of DNA to Form RNA Decreased Catabolism of Protein and Amino Acids Summary Growth Hormone Enhances Fat Utilization for Energy “Ketogenic” Effect of Excessive Growth Hormone Growth Hormone Decreases Carbohydrate Utilization Necessity of Insulin and Carbohydrate for the Growth­Promoting Action of Growth Hormone GROWTH HORMONE STIMULATES CARTILAGE AND BONE GROWTH GROWTH HORMONE EXERTS MUCH OF ITS EFFECT THROUGH INSULIN-LIKE GROWTH FACTORS (SOMATOMEDINS) Short Duration of Action of Growth Hormone but Prolonged Action of IGF-1 REGULATION OF GROWTH HORMONE SECRETION Hypothalamic Growth Hormone–Releasing Hormone Stimulates, and Somatostatin Inhibits Growth Hormone Secretion Posterior Pituitary Gland and its Relation to the Hypothalamus PHYSIOLOGICAL FUNCTIONS OF ANTIDIURETIC HORMONE Regulation of Antidiuretic Hormone Production Increased Extracellular Fluid Osmolarity Stimulates ADH Secretion Low Blood Volume and Low Blood Pressure Stimulate ADH Secretion—Vasoconstrictor Effects of ADH Physiological Functions of Oxytocin Oxytocin Causes Contraction of the Pregnant Uterus Oxytocin Aids in Milk Ejection by the Breasts Bibliography Chapter 77: Thyroid Metabolic Hormones Synthesis and Secretion of the Thyroid Metabolic Hormones PHYSIOLOGIC ANATOMY OF THE THYROID GLAND IODINE IS REQUIRED FOR THYROXINE FORMATION Fate of Ingested Iodides IODIDE PUMP—THE SODIUM-IODIDE SYMPORTER (IODIDE TRAPPING) Thyroglobulin and Formation of Thyroxine and Triiodothyronine Formation and Secretion of Thyroglobulin by the Thyroid Cells Oxidation of the Iodide Ion Iodination of Tyrosine and Thyroid Hormone Formation—“Organification” of Thyroglobulin Storage of Thyroglobulin RELEASE OF THYROXINE AND TRIIODOTHYRONINE FROM THE THYROID GLAND Daily Rate of Secretion of Thyroxine and Triiodothyronine Transport of Thyroxine and Triiodothyronine to Tissues Thyroxine and Triiodothyronine Are Bound to Plasma Proteins Thyroxine and Triiodothyronine Are Released Slowly to Tissue Cells Thyroid Hormones Have Slow Onset and Long Duration of Action PHYSIOLOGICAL FUNCTIONS OF THE THYROID HORMONES Thyroid Hormones Increase Transcription of Many Genes Most of the Thyroxine Secreted by the Thyroid Is Converted to Triiodothyronine Thyroid Hormones Activate Nuclear Receptors THYROID HORMONES INCREASE CELLULAR METABOLIC ACTIVITY Thyroid Hormones Increase the Number and Activity of Mitochondria Thyroid Hormones Increase Active Transport of Ions Through Cell Membranes Effects of Thyroid Hormone on Specific Body Functions Stimulation of Carbohydrate Metabolism Stimulation of Fat Metabolism Effect on Plasma and Liver Fats Increased Requirement for Vitamins Increased Basal Metabolic Rate Decreased Body Weight Increased Blood Flow and Cardiac Output Increased Heart Rate Increased Heart Strength Normal Arterial Pressure Increased Respiration Increased Gastrointestinal Motility Excitatory Effects on the Central Nervous System Effect on the Function of the Muscles Muscle Tremor Effect on Sleep Effect on Other Endocrine Glands Effect of Thyroid Hormone on Sexual Function Regulation of Thyroid Hormone Secretion TSH (FROM THE ANTERIOR PITUITARY GLAND) INCREASES THYROID SECRETION Cyclic Adenosine Monophosphate Mediates the Stimulatory Effect of TSH ANTERIOR PITUITARY SECRETION OF TSH IS REGULATED BY THYROTROPIN-RELEASING HORMONE FROM THE HYPOTHALAMUS Effects of Cold and Other Neurogenic Stimuli on TRH and TSH Secretion FEEDBACK EFFECT OF THYROID HORMONE TO DECREASE ANTERIOR PITUITARY SECRETION OF TSH Bibliography Chapter 78: Adrenocortical Hormones Corticosteroids: Mineralocorticoids, Glucocorticoids, and Androgens SYNTHESIS AND SECRETION OF ADRENOCORTICAL HORMONES The Adrenal Cortex has Three Distinct Layers FUNCTIONS OF MINERALOCORTICOIDS—ALDOSTERONE Mineralocorticoid Deficiency Causes Severe Renal Sodium Chloride Wasting and Hyperkalemia Aldosterone Is the Major Mineralocorticoid Secreted by the Adrenals Renal and Circulatory Effects of Aldosterone Aldosterone Increases Renal Tubular Reabsorption of Sodium and Secretion of Potassium Excess Aldosterone Increases Extracellular Fluid Volume and Arterial Pressure But Has Only a Small Effect on Plasma Sodium Concentration; Aldosterone Deficiency Causes Hyponatremia Excess Aldosterone Causes Hypokalemia and Muscle Weakness; Aldosterone Deficiency Causes Hyperkalemia and Cardiac Toxicity Excess Aldosterone Increases Tubular Hydrogen Ion Secretion and Causes Alkalosis ALDOSTERONE STIMULATES SODIUM AND POTASSIUM TRANSPORT IN SWEAT GLANDS, SALIVARY GLANDS, AND INTESTINAL EPITHELIAL CELLS CELLULAR MECHANISM OF ALDOSTERONE ACTION POSSIBLE NONGENOMIC ACTIONS OF ALDOSTERONE AND OTHER STEROID HORMONES REGULATION OF ALDOSTERONE SECRETION Functions of Glucocorticoids Effects of Cortisol on Carbohydrate Metabolism Stimulation of Gluconeogenesis Decreased Glucose Utilization by Cells Elevated Blood Glucose Concentration and “Adrenal Diabetes” Effects of Cortisol on Protein Metabolism Reduction in Cellular Protein Cortisol Increases Liver and Plasma Proteins Increased Blood Amino Acids, Diminished Transport of Amino Acids Into Extrahepatic Cells, and Enhanced Transport Into Hepatic Cells Effects of Cortisol on Fat Metabolism Mobilization of Fatty Acids Excess Cortisol Causes Obesity CORTISOL IS IMPORTANT IN RESISTING STRESS AND INFLAMMATION Anti­inflammatory Effects of High Levels of Cortisol Cortisol Prevents the Development of Inflammation by Stabilizing Lysosomes and by Other Effects Cortisol Causes Resolution of Inflammation Regulation of Cortisol Secretion by Adrenocorticotropic Hormone from the Pituitary Gland ACTH Stimulates Cortisol Secretion Chemistry of ACTH ACTH Secretion Is Controlled by Corticotropin­Releasing Factor From the Hypothalamus ACTH Activates Adrenocortical Cells to Produce Steroids by Increasing cAMP Physiological Stress Increases ACTH and Adrenocortical Secretion Inhibitory Effect of Cortisol on the Hypothalamus and Anterior Pituitary to Decrease ACTH Secretion. Summary of the Cortisol Control System Synthesis and Secretion of ACTH in Association With Melanocyte­Stimulating Hormone, Lipotropin, and Endorphin Bibliography Chapter 79: Insulin, Glucagon, and Diabetes Mellitus Insulin and its Metabolic Effects INSULIN IS A HORMONE ASSOCIATED WITH ENERGY ABUNDANCE INSULIN CHEMISTRY AND SYNTHESIS ACTIVATION OF TARGET CELL RECEPTORS BY INSULIN AND THE RESULTING CELLULAR EFFECTS EFFECT OF INSULIN ON CARBOHYDRATE METABOLISM Insulin Promotes Muscle Glucose Uptake and Metabolism Storage of Glycogen in Muscle Quantitative Effect of Insulin to Facilitate Glucose Transport Through the Muscle Cell Membrane Insulin Promotes Liver Uptake, Storage, and Use of Glucose Glucose Is Released From the Liver Between Meals Insulin Promotes Conversion of Excess Glucose Into Fatty Acids and Inhibits Gluconeogenesis in the Liver Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain Effect of Insulin on Carbohydrate Metabolism in Other Cells Effect of Insulin on Fat Metabolism Insulin Promotes Fat Synthesis and Storage Role of Insulin in Storage of Fat in the Adipose Cells Insulin Deficiency Increases Use of Fat for Energy Insulin Deficiency Causes Lipolysis of Storage Fat and Release of Free Fatty Acids Insulin Deficiency Increases Plasma Cholesterol and Phospholipid Concentrations Excess Usage of Fats During Insulin Deficiency Causes Ketosis and Acidosis Effect of Insulin on Protein Metabolism and Growth Insulin Promotes Protein Synthesis and Storage Insulin Deficiency Causes Protein Depletion and Increased Plasma Amino Acids Insulin and Growth Hormone Interact Synergistically to Promote Growth Mechanisms of Insulin Secretion Control of Insulin Secretion Increased Blood Glucose Stimulates Insulin Secretion Feedback Relation Between Blood Glucose Concentration and the Insulin Secretion Rate THE ROLE OF INSULIN (AND OTHER HORMONES) IN “SWITCHING” BETWEEN CARBOHYDRATE AND LIPID METABOLISM Glucagon and its Functions Effects on Glucose Metabolism Glucagon Causes Glycogenolysis and Increased Blood Glucose Concentration Glucagon Increases Gluconeogenesis Other Effects of Glucagon Regulation of Glucagon Secretion Increased Blood Glucose Inhibits Glucagon Secretion Increased Blood Amino Acids Stimulate Secretion of Glucagon Exercise Stimulates Secretion of Glucagon Summary of Blood Glucose Regulation Importance of Blood Glucose Regulation Bibliography Chapter 80: Parathyroid Hormone, Calcitonin, Calcium and Phosphate Metabolism, Vitamin D, Bone, and Teeth Overview of Calcium and Phosphate Regulation in Extracellular Fluid and Plasma CALCIUM IN THE PLASMA AND INTERSTITIAL FLUID INORGANIC PHOSPHATE IN THE EXTRACELLULAR FLUIDS NONBONE PHYSIOLOGICAL EFFECTS OF ALTERED CALCIUM AND PHOSPHATE CONCENTRATIONS IN THE BODY FLUIDS Hypocalcemia Causes Nervous System Excitement and Tetany Hypercalcemia Depresses Nervous System and Muscle Activity Absorption and Excretion of Calcium and Phosphate Intestinal Absorption and Fecal Excretion of Calcium and Phosphate Renal Excretion of Calcium and Phosphate Bone and its Relationship to Extracellular Calcium and Phosphate Organic Matrix of Bone Bone Salts Tensile and Compressional Strength of Bone Precipitation and Absorption of Calcium and Phosphate in Bone—Equilibrium With the Extracellular Fluids Hydroxyapatite Does Not Precipitate in Extracellular Fluid Despite Supersaturation of Calcium and Phosphate Ions Mechanism of Bone Calcification Precipitation of Calcium in Nonosseous Tissues Under Abnormal Conditions CALCIUM EXCHANGE BETWEEN BONE AND EXTRACELLULAR FLUID Deposition and Resorption of Bone—Remodeling of Bone Deposition of Bone by the Osteoblasts Resorption of Bone—Function of the Osteoclasts Bone Deposition and Resorption Are Normally in Equilibrium Value of Continual Bone Remodeling Control of the Rate of Bone Deposition by Bone “Stress” Vitamin D Cholecalciferol (Vitamin D3) Is Formed in the Skin Cholecalciferol Is Converted to 25­Hydroxycholecalciferol in the Liver Formation of 1,25­Dihydroxycholecalciferol in the Kidneys and Its Control by Parathyroid Hormone Calcium Ion Concentration Controls the Formation of 1,25­Dihydroxycholecalciferol Actions of Vitamin D “Hormonal” Effect of Vitamin D to Promote Intestinal Calcium Absorption Vitamin D Promotes Phosphate Absorption by the Intestines Vitamin D Decreases Renal Calcium and Phosphate Excretion Effect of Vitamin D on Bone and Its Relation to Parathyroid Hormone Activity Parathyroid Hormone PARATHYROID HORMONE EFFECTS ON EXTRACELLULAR FLUID CALCIUM AND PHOSPHATE CONCENTRATIONS Parathyroid Hormone Mobilizes Calcium and Phosphate From Bone Rapid Phase of Calcium and Phosphate Mobilization From Bone—Osteolysis Slow Phase of Bone Resorption and Calcium Phosphate Release—Activation of the Osteoclasts Parathyroid Hormone Decreases Calcium Excretion and Increases Phosphate Excretion by the Kidneys Parathyroid Hormone Increases Intestinal Absorption of Calcium and Phosphate Cyclic Adenosine Monophosphate Mediates the Effects of Parathyroid Hormone CONTROL OF PARATHYROID SECRETION BY CALCIUM ION CONCENTRATION SUMMARY OF EFFECTS OF PARATHYROID HORMONE Calcitonin Increased Plasma Calcium Concentration Stimulates Calcitonin Secretion Calcitonin Decreases Plasma Calcium Concentration Calcitonin Has a Weak Effect on Plasma Calcium Concentration in Adult Humans Summary of Control of Calcium ion Concentration Buffer Function of the Exchangeable Calcium in Bones—The First Line of Defense Hormonal Control of Calcium Ion Concentration—The Second Line of Defense Physiology of the Teeth FUNCTION OF THE DIFFERENT PARTS OF THE TEETH Enamel Dentin Cementum Pulp Dentition Formation of the Teeth Eruption of Teeth Development of the Permanent Teeth Metabolic Factors Influence Development of the Teeth Mineral Exchange in Teeth Bibliography Chapter 81: Reproductive and Hormonal Functions of the Male (and Function of the Pineal Gland) Spermatogenesis Steps of Spermatogenesis Meiosis Sex Chromosomes Formation of Sperm Hormonal Factors That Stimulate Spermatogenesis Maturation of Sperm in the Epididymis Storage of Sperm in the Testes Physiology of the Mature Sperm Function of the Seminal Vesicles Function of the Prostate Gland Semen “Capacitation” of Spermatozoa Is Required for Fertilization of the Ovum Acrosome Enzymes, the “Acrosome Reaction,” and Penetration of the Ovum Why Does Only One Sperm Enter the Oocyte? Male Sexual Act Neuronal Stimulus for Performance of the Male Sexual Act Psychic Element of Male Sexual Stimulation Integration of the Male Sexual Act in the Spinal Cord Stages of the Male Sexual Act Penile Erection—Role of the Parasympathetic Nerves Lubrication Is a Parasympathetic Function Emission and Ejaculation Are Functions of the Sympathetic Nerves TESTOSTERONE AND OTHER MALE SEX HORMONES Secretion, Metabolism, and Chemistry of the Male Sex Hormones Secretion of Testosterone by the Interstitial Cells of Leydig in the Testes Functions of Testosterone Functions of Testosterone During Fetal Development Effect of Testosterone to Cause Descent of the Testes Effect of Testosterone on Development of Adult Primary and Secondary Sexual Characteristics Effect on the Distribution of Body Hair Male Pattern Baldness Effect on the Voice Testosterone Increases Thickness of the Skin and Can Contribute to Development of Acne Testosterone Increases Protein Formation and Muscle Development Testosterone Increases Bone Matrix and Causes Calcium Retention Testosterone Increases the Basal Metabolic Rate Testosterone Increases Red Blood Cells Effect on Electrolyte and Water Balance BASIC INTRACELLULAR MECHANISM OF ACTION OF TESTOSTERONE CONTROL OF MALE SEXUAL FUNCTIONS BY HORMONES FROM THE HYPOTHALAMUS AND ANTERIOR PITUITARY GLAND Gonadotropin­Releasing Hormone Increases Secretion of Luteinizing Hormone and Follicle­Stimulating Hormone Gonadotropic Hormones: Luteinizing Hormone and Follicle­Stimulating Hormone Regulation of Testosterone Production by Luteinizing Hormone Inhibition of Anterior Pituitary Secretion of Luteinizing and Follicle­Stimulating Hormones by Testosterone—Negative Feedback Control of Testosterone Secretion Regulation of Spermatogenesis by Follicle­Stimulating Hormone and Testosterone Role of Inhibin in Negative Feedback Control of Seminiferous Tubule Activity Human Chorionic Gonadotropin Secreted by the Placenta During Pregnancy Stimulates Testosterone Secretion by the Fetal Testes Puberty and Regulation of Its Onset Bibliography Chapter 82: Female Physiology Before Pregnancy and Female Hormones Physiologic Anatomy of the Female Sexual Organs Oogenesis and Follicular Development in the Ovaries Female Hormonal System Monthly Ovarian Cycle and Function of Gonadotropic Hormones GONADOTROPIC HORMONES AND THEIR EFFECTS ON THE OVARIES OVARIAN FOLLICLE GROWTH—THEF OLLICULAR PHASE OF THE OVARIAN CYCLE Development of Antral and Vesicular Follicles Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia Ovulation A Surge of Luteinizing Hormone Is Necessary for Ovulation Initiation of Ovulation CORPUS LUTEUM—THE LUTEAL PHASE OF THE OVARIAN CYCLE Luteinizing Function of Luteinizing Hormone Secretion by the Corpus Luteum: An Additional Function of Luteinizing Hormone Involution of the Corpus Luteum and Onset of the Next Ovarian Cycle Summary Functions of Ovarian Hormones—Estradiol and Progesterone Chemistry of the Sex Hormones Estrogens Progestins Synthesis of the Estrogens and Progestins Estrogens and Progesterone Are Transported in the Blood Bound to Plasma Proteins Functions of the Liver in Estrogen Degradation Fate of Progesterone FUNCTIONS OF THE ESTROGENS—THEIR EFFECTS ON THE PRIMARY AND SECONDARY FEMALE SEX CHARACTERISTICS Effect of Estrogens on the Uterus and External Female Sex Organs Effect of Estrogens on the Fallopian Tubes Effect of Estrogens on the Breasts Effect of Estrogens on the Skeleton Osteoporosis of the Bones Caused by Estrogen Deficiency in Old Age Estrogens Slightly Increase Protein Deposition Estrogens Increase Body Metabolism and Fat Deposition Estrogens Have Little Effect on Hair Distribution Effect of Estrogens on the Skin Effect of Estrogens on Electrolyte Balance Functions of Progesterone Progesterone Promotes Secretory Changes in the Uterus Progesterone Promotes Secretion by the Fallopian Tubes Progesterone Promotes Development of the Breasts MONTHLY ENDOMETRIAL CYCLE AND MENSTRUATION Proliferative Phase (Estrogen Phase) of the Endometrial Cycle Occurs Before Ovulation Secretory Phase (Progestational Phase) of the Endometrial Cycle Occurs After Ovulation Menstruation Leukorrhea During Menstruation Regulation of Female Monthly Rhythm—Interplay Between Ovarian and Hypothalamic­Pituitary Hormones THE HYPOTHALAMUS SECRETES GNRH, WHICH STIMULATES THE ANTERIOR PITUITARY GLAND TO SECRETE LH AND FSH Intermittent, Pulsatile Secretion of GnRH by the Hypothalamus Stimulates Pulsatile Release of LH From the Anterior Pituitary Gland Hypothalamic Centers for Release of Gonadotropin­Releasing Hormone NEGATIVE FEEDBACK EFFECTS OF ESTROGEN AND PROGESTERONE TO DECREASE LH AND FSH SECRETION Inhibin From the Corpus Luteum Inhibits FSH and LH Secretion POSITIVE FEEDBACK EFFECT OF ESTROGEN BEFORE OVULATION—THE PREOVULATORY LUTEINIZING HORMONE SURGE FEEDBACK OSCILLATION OF THE HYPOTHALAMIC-PITUITARY-OVARIAN SYSTEM Anovulatory Cycles—Sexual Cycles at Puberty Puberty and Menarche Menopause Female Sexual Act Stimulation of the Female Sexual Act Female Erection and Lubrication Female Orgasm Bibliography Chapter 83: Pregnancy and Lactation Maturation and Fertilization of the Ovum Entry of the Ovum Into the Fallopian Tube (Uterine Tube) Fertilization of the Ovum WHAT DETERMINES THE SEX OF THE FETUS THAT IS CREATED? TRANSPORT OF THE FERTILIZED OVUM IN THE FALLOPIAN TUBE IMPLANTATION OF THE BLASTOCYST IN THE UTERUS Early Nutrition of the Embryo Anatomy and Function of the Placenta PLACENTAL PERMEABILITY AND MEMBRANE DIFFUSION CONDUCTANCE Diffusion of Oxygen Through the Placental Membrane Diffusion of Carbon Dioxide Through the Placental Membrane Diffusion of Foodstuffs Through the Placental Membrane Excretion of Waste Products Through the Placental Membrane Hormonal Factors in Pregnancy HUMAN CHORIONIC GONADOTROPIN CAUSES PERSISTENCE OF THE CORPUS LUTEUM AND PREVENTS MENSTRUATION Function of Human Chorionic Gonadotropin Human Chorionic Gonadotropin Stimulates the Male Fetal Testes to Produce Testosterone SECRETION OF ESTROGENS BY THE PLACENTA Function of Estrogen in Pregnancy SECRETION OF PROGESTERONE BY THE PLACENTA HUMAN CHORIONIC SOMATOMAMMOTROPIN Parturition Increased Uterine Excitability Near Term Hormonal Factors That Increase Uterine Contractility Increased Ratio of Estrogens to Progesterone Oxytocin Causes Contraction of the Uterus Effect of Fetal Hormones on the Uterus Mechanical Factors That Increase Uterine Contractility Stretch or Irritation of the Cervix ONSET OF LABOR—A POSITIVE FEEDBACK MECHANISM FOR ITS INITIATION ABDOMINAL MUSCLE CONTRACTIONS DURING LABOR Lactation Development of the Breasts Estrogens Stimulate Growth of the Ductal System of the Breasts Progesterone Is Required for Full Development of the Lobule­Alveolar System Prolactin Promotes Lactation The Hypothalamus Secretes Prolactin Inhibitory Hormone Suppression of the Female Ovarian Cycles in Nursing Mothers for Many Months After Delivery EJECTION (OR “LET-DOWN”) PROCESS IN MILK SECRETION—FUNCTION OF OXYTOCIN Inhibition of Milk Ejection MILK COMPOSITION AND THE METABOLIC DRAIN ON THE MOTHER CAUSED BY LACTATION Antibodies and Other Anti­infectious Agents in Milk Bibliography Chapter 84: Fetal and Neonatal Physiology Bibliography Unit XV: Sports Physiology Chapter 85: Sports Physiology Bibliography Normal Values for Selected Common Laboratory Measurements