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Experimental Coronary Disease Models and Methods of Drug Evaluation.- A. Introduction.- I. Definitions.- II. Common Role of Subendocardial Ischemia.- III. Objective of the Presentation.- B. Pathophysiology of Myocardial Ischemia.- I. Regulation of Tissue Oxygen Tension (pO2).- II. Autoregulation.- III. Effect of Antianginal Drugs.- C. Subendocardium and Effect of Drugs.- I. Anatomy of Circulation through Left Ventricular Wall.- II. Basal State of Left Ventricular Subepicardium and Subendocardium.- D. Regional Resistance Large and Small Coronary Arteries.- I. Quantitative Angiography.- II. Large and Small Arteries in vivo.- III. Large and Small Arteries in vitro.- E. Regional Tissue Oxygen Tension.- I. Principle and Determinants of Oxygen Tension.- II. Approaches.- III. Polarographic Method.- IV. Mass Spectrographic Method.- V. Conclusions Regional Oxygen Tension.- F. Regional Blood Flow and Perfusion.- I. Epicardium and Endocardium.- II. Microsphere Method.- III. Hydrogen Clearance with Electrodes.- IV. Mass Spectrometer.- V. Conclusions Regional Flow.- G. Other Methods for Measurement of Coronary Blood Flow.- I. Thermodilution.- II. Heat Dissipation and Heat Production.- H. Blood Flow and Metabolism of Ischemic Region.- I. Retrograde Blood Flow (Back Flow).- II. Collateral Flow and Metabolism of Ischemic Region.- III. Collateral Flow in Unanesthetized Dogs.- I. Atherosclerosis Model.- Atrial Pacing.- J. Diffuse Coronary Occlusion Small Vessels.- I. Ischemic Heart Failure and Cardiogenic Shock by Starch Suspensions, Lycopodium Spores or Small Microspheres.- II. Large Spheres Intra-Aortic.- K. Acute Ligation.- I. Two-Stage Ligation in the Anesthetized Dog.- II. Two-Stage Ligation in the Anesthetized Pig.- III. Monkey, Unanesthetized.- L. Gradual or Controlled Occlusion.- I. Ameroids.- II. Dicetyl Phosphate.- III. Inflatable Balloon.- IV. Hydraulic Occluders.- V. Intracoronary Balloon.- M. Gradual or Acute Thrombosis.- I. Spiral Coils.- II. Electric Induction of Thrombosis.- III. Magnet and Iron Particles.- N. Other Means of Occlusion.- I. Mercury Injection into Coronary.- II. Steel Balls into Coronary.- III. Lead Foil into Coronary.- IV. Steel Cylinder in Coronary.- V. Catheter Tip in Coronary.- VI. Wedging Catheter in Coronary.- O. Surface Electrograms after Occlusion.- I. Electrograms in Open-Chest Dogs.- II. Closed-Chest Conscious Dogs.- P. Contractility of Ischemic Zone.- Q. Partial Occlusion and Pacing in Dog.- R. Summary and Conclusions.- References.- Experimental Induction of Hypertension.- A. Introduction.- B. Experimental Induction of Essential Hypertension.- I. Spontaneous Genetically Determined Hypertension.- II. Teratogenic Induction of Hypertension.- C. Surgical Induction of Chronic Sustained Diastolic Hypertension.- I. The Goldblatt Procedure.- II. Other Procedures for Constricting the Renal Artery.- III. Application of a Figure-of-Eight Ligature.- IV. Infarction of the Kidney.- V. Adrenal Regeneration Hypertension.- VI. Miscellaneous Surgical Procedures.- D. Non-Surgical Procedures for Inducing Experimental Chronic Diastolic Hypertension.- I. Salt-Induced Hypertension.- II. DOCA-Induced Hypertension.- III. Hypertension Induced by Dietary Deficiencies.- E. Induction of Special Forms of Hypertension.- I. Systolic Hypertension.- II. Hypertension Secondary to Nephritis and Nephrosclerosis.- III. Surgically Remediable Hypertension.- IV. Renoprival Hypertension.- V. Neurogenic Hypertension.- VI. Malignant Hypertension.- F. Other Procedures for Inducing Experimental Hypertension.- I. Induction of Hypertension by Steroids and Other Hormones.- II. Induction of Hypertension by Other Drugs and Poisons.- III. Induction of Hypertension by Activation of the Immune Mechanism.- G. Conclusion.- References.- Experimental Production of Atherosclerosis: Nutritional Influences.- A. Introduction.- B. The Peanut Oil Problem.- C. Dietary-Induced Cerebral Atherosclerosis.- D. Recent Atherosclerosis-Regression Studies (Aorta and Coronary Artery Only).- E. Lessons from Animal Experiments in Diabetes and Atherosclerosis.- F. Polyunsaturated Fatty Acid Diet and Cancer From the Experimental and Epidemiological Viewpoint.- G. The Soft and Hard Water Hypothesis in Atherogenesis From the Combined Experimental-Epidemiological Viewpoint.- H. The Issue of Coffee-Caffeine Administration and Atherogenesis of the Aorta and the Coronary Arteries.- I. Pointers from Animal Experiments on Vitamin D Toxicity.- J. Disturbance of Lipid Metabolism in Animals with Brominated Vegetable Oils.- References.- Production of Myocardial Infarcts in Animal Experiments.- A. Historical Background.- B. Methods for Production of Complete or Partial Obstruction of Coronary Arteries.- I. Ligation of Coronary Arteries.- II. Methods of Producing Complete or Partial Occlusion by Means of Clips, Cuffs, Balloons, Screw Forceps, Snares, and Intracranial Arterial Clamps.- III. Occlusion by Means of Embolization and Thrombosis.- IV. Progressive Obstruction Resulting from Application of Ameroid Clamps.- V. Experimental Production of Atherosclerosis through Diet.- References.- Experimental Cardiac Arrhythmias.- A. Introduction.- B. Production of Cardiac Arrhythmias by Electrical Stimulation of the Heart.- I. Single Electrical Shock.- II. Serial Electrical Shocks of Progressively Increasing Intensity.- III. Electrical Stimulation of Continuously Increasing Frequency Rate.- IV. Prolonged Application of Galvanic Current.- C. Cardiac Arrhythmias Evoked by Local Blocks and Spontaneously Firing Ectopic Foci Produced by Local Myocardial Ischemia and Thermal or Mechanical Injury of the Myocardium.- I. Local Myocardial Ischemia.- II. Local Heating or Cooling of the Myocardium.- III. Mechanical Injury of the Myocardium.- D. Induction of Cardiac Arrhythmias by Intravenous Administration or Topical Application of Drugs or Other Chemical Substances.- I. Intravenous Administration of Arrhythmogenic Agents.- 1. Administration of One Arrhythmogenic Agent.- 2. Combined Administration of Several Arrhythmogenic Agents.- II. Topical Application of Arrhythmogenic Agents to the Heart.- E. Production of Cardiac Arrhythmias by Direct Stimulation of the Central Nervous System.- I. Electrical Stimulation of the Central Nervous System.- II. Injection of Drugs or Other Chemical Substances into the Cerebral Ventricles.- III. Increased Intracranial Pressure or Cerebral Compression.- References.- Experimental Production of Cerebral Vascular Disorders.- A. Introduction.- B. Acute Experimental Occlusion.- C. Dysregulation of the Intracerebral Blood Distribution.- D. Effect of Decreased CBF on Cerebral Tissue Energetics.- E. Blood Pressure and Disturbance of the Cerebral Vascular Autoregulation.- F. Changes in Cerebral Activity and Cerebral Blood Flow.- G. Nervous Influences on Cerebral Vessels.- Stimulation and Blockade of the Cervical Autonomic Nerves.- H. Experimental Investigation of the Smooth Muscles of Brain Vessels.- I. Disturbances of CBF by Variation of Blood Gases.- I. Increase in CO2 and CBF.- II. Hypoxia and CBF.- III. Hyperventilation and CBF.- J. Variations of Intracranial Volume and Cerebral Blood Flow.- K. Conclusion.- References.- Experimental Production of Pulmonary Hypertension.- A. Introduction.- B. Pathophysiological Background of the Pulmonary Circulation.- C. Vascular Changes in Pulmonary Hypertension.- D. Methods for the Production of Experimental Pulmonary Hypertension.- I. The Production of Vasoconstriction in the Pulmonary Vascular Bed.- II. Effects of Embolization on the Pulmonary Vascular Bed.- III. Production of Functional Mitral Stenosis.- IV. Production of Hyperkinetic Pulmonary Hypertension.- V. Production of Pulmonary Hypertension Due to Environmental Influence.- VI. Pulmonary Hypertension in Transplantation.- E. Conclusions.- References.- Experimentally Induced Changes in Pulmonary Circulation.- A. Introduction.- B. Morphology and Physiology of the Pulmonary Capillary System.- I. Inne…