Whenever the coronary flow is inadequate to provide enough oxygen to meet the energy demands of the tissue, the heart becomes ischemic. Manifestations of myocardial ischemia include depression in contractile activity, changes in metabolic pattern, abnormalities in ultrastructure, and alterations in membrane potential. Ischemic changes during the early phase are reversible but as the period of ischemia is extended, the injury becomes irreversible. The transition from reversible to irreversible ischemic injury is usually associated with some membrane defects. It is worthwhile to consider that the irreversible damage to the ischemic myocardium occurs when the sarcolemmal membrane is altered in suoh a way that it would promote 2 a net gain of ca + in the cardiac cell upon reinstitution of blood flow. Suoh a lesion could result when mechanisms for the entry as well as removal 2 of ca + from the myocardial oell become defective. In this regard, 2 depression of the sarcolemmal ca + pump would favour the oocurrenoe of 2 intracellular ca + overload. Furthermore, inhibition of the Na+-K+ pump would lead to elevation of myoplasmic Na+ which oould then increase the 2 2 intracellular concentration of ca + through the sarcolemmal Na+-ca + exchange mechanism. In faot recent studies have revealed an inhibition of 2 the sarcolemmal Na+-ca + exchange mechanism in the ischemic heart and this 2 change could also contribute towards the occurrence of intracellular ca + 2 overload.
Table of ContentsMyocardial Cell Damage and Arrhythmias.- Ultrastructural Abnormalities in Ischemic Heart Disease.- Preconditioning with Ischemia: A Means to Delay Cell Death in Ischemic Myocardium.- Modification of the Thromboxane/Prostacyclin Balance as an Approach to Antiarrhythmic Therapy During Myocardial Ischaemia and Reperfusion; The Concept of Endogenous Antiarrhythmic Substances.- Mechanisms of Coupled Arrhythmias in Guinea Pig Perfused Heart and Isolated Ventricular Tissue Models of Ischemia-Reperfusion.- The Preventive Effect of Sodium Selenite Against Ischemic Ventricular Arrhythmia and Some Clues to its Mechanisms.- Pathophysiologic Aspects of Ischemic Injury.- Molecular Events Occurring During Post-Ischaemic Reperfusion.- Oxidation of Methionine in Proteins of Isolated Rat Heart Myocytes and Tissue Slices by Neutrophil-Generated Oxygen Free Radicals.- Phospholipid Metabolism in Heart Membranes.- Models of Injury of Cardiovascular Membranes by Amphiphiles and Free Radicals.- Inability of Superoxide Dismutase and Catalase to Inhibit Calcium Influx on Reoxygenation of Rabbit Myocardium.- Catecholamine Release in Myocardial Ischemia and Its Clinical Implications.- Coronary Blood Flow in Myocardial Stress with Catecholamine Administration in the Dog.- Morphometric Analysis of Regional Myocardial Perfusion in Rats as Measured by Non-Radioactive Microspheres.- Prostaglandins and Defects in Vascular Function.- Endothelium Dependent Relaxation and Atherosclerosis.- Metabolic Aspects of Cell Damage.- Energy Metabolism in Myocardial Ischemia and Reperfusion.- The Role of Beta-Adrenoceptors in Ischemia-Induced Acidosis in the Isolated Rat Heart : A 31-P NMR Study.- Protective and Nonprotective Effects of Drugs on Cardiac Contractile Activity and High Energy Phosphates During Anoxia and After Reoxygenation.- Myocardial Enzyme Leakage and Succinic Dehydrogenase Activity of Mitochondria Correlated with the Morphological Changes in the Anoxic Isolated Perfused Rat Heart.- Hemodynamic Performance of Isolated Blood-Perfused Working Hearts of Creatine Depleted Rats in Hypoxemia.- Phosphorus Nuclear Magnetic Resonance Measurements of Intracellular pH in Isolated Rabbit Heart During the Calcium Paradox.- Hypercontracture of Isolated Adult Rat Heart Myocytes: Multiple Causes and a Common Mechanism.- Mechanical Restitution and Inotropic Reserve of the Rat Heart Following Heterothermal Global Ischemia.- Calcium Antagonists and Myocardial Ischemia.- Calcium Antagonism and the Ischemic Myocardium.- Biochemical and Ultrastructural Alterations in Cardiac Membranes During Ischaemia-Reperfusion: Protection by a Calcium Entry Blocker.- Effect of Nifedipine and Hyaluronidase Alone and in Combination on Myocardial Preservation in Experimental Myocardial Infarction A Morphological and Biochemical Profile.- Action of Calcium Antagonists on the Contraction of Isolated Human Coronary Arteries and Myocardium.- Inhibitory Effects of Allicin (Diallyl Disulfide-Oxide, A Constituent of Garlic Oil) on Human Platelet and Polymorphonuclear Leukocyte Function.