Myocardial Ischemia

1. Front Matter

   Pages i-xiv

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2. Myocardial Cell Damage and Arrhythmias

   1. Front Matter

      Pages 1-1

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   2. Ultrastructural Abnormalities in Ischemic Heart Disease

      • Jutta Schaper

      Pages 3-9

   3. Preconditioning with Ischemia: A Means to Delay Cell Death in Ischemic Myocardium

      • Charles E. Murry, Robert B. Jennings, Keith A. Reimer

      Pages 11-20

   4. Modification of the Thromboxane/Prostacyclin Balance as an Approach to Antiarrhythmic Therapy During Myocardial Ischaemia and Reperfusion; The Concept of Endogenous Antiarrhythmic Substances

      • James R. Parratt

      Pages 21-35

   5. Mechanisms of Coupled Arrhythmias in Guinea Pig Perfused Heart and Isolated Ventricular Tissue Models of Ischemia-Reperfusion

      • Gregory R. Ferrier, C. M. Guyette

      Pages 37-51

   6. The Preventive Effect of Sodium Selenite Against Ischemic Ventricular Arrhythmia and Some Clues to its Mechanisms

      • Y. A. Mei, Y. Q. Xu, H. D. Zhang

      Pages 53-63

3. Pathophysiologic Aspects of Ischemic Injury

   1. Front Matter

      Pages 65-65

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   2. Molecular Events Occurring During Post-Ischaemic Reperfusion

      • R. Ferrari, C. Ceconi, S. Curello, A. Cargnoni, A. Albertini, E. O. Visioli

      Pages 67-84

   3. Oxidation of Methionine in Proteins of Isolated Rat Heart Myocytes and Tissue Slices by Neutrophil-Generated Oxygen Free Radicals

      • H. Fliss, G. Docherty

      Pages 85-98

   4. Phospholipid Metabolism in Heart Membranes

      • K. J. Kako, M. Kato

      Pages 99-112

   5. Models of Injury of Cardiovascular Membranes by Amphiphiles and Free Radicals

      • W. B. Weglicki, I. T. Mak, B. F. Dickens, J. H. Kramer

      Pages 113-122

   6. Inability of Superoxide Dismutase and Catalase to Inhibit Calcium Influx on Reoxygenation of Rabbit Myocardium

      • P. A. Poole-Wilson, M. A. Tones

      Pages 123-131

   7. Catecholamine Release in Myocardial Ischemia and Its Clinical Implications

      • W. Kübler, R. Dietz, W. Mäurer, A. Schömig

      Pages 133-143

   8. Coronary Blood Flow in Myocardial Stress with Catecholamine Administration in the Dog

      • R. M. Berne, J. M. Gidday, H. E. Hill, R. Rubio

      Pages 145-148

   9. Morphometric Analysis of Regional Myocardial Perfusion in Rats as Measured by Non-Radioactive Microspheres

      • M. Korpan, K. Rakusan

      Pages 149-161

   10. Prostaglandins and Defects in Vascular Function

       • Dennis B. McNamara, John A. Bellan, Philip R. Mayeux, Morris D. Kerstein, Albert L. Hyman, Philip J. Kadowitz et al.

       Pages 163-170

   11. Endothelium Dependent Relaxation and Atherosclerosis

       • N. Sreeharan, R. Jayakody, M. Senaratne, A. Thomson, T. Kappagoda

       Pages 171-182

4. Metabolic Aspects of Cell Damage

   1. Front Matter

      Pages 183-183

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   2. Energy Metabolism in Myocardial Ischemia and Reperfusion

      • Robert B. Jennings, Keith A. Reimer, Charles Steenbergen, Charles E. Murry

      Pages 185-198

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.

• arrhythmia
• artery
• atherosclerosis
• blood
• cardiovascular
• cell
• depression
• drugs
• energy
• heart
• heart disease
• myocardial infarction
• platelet
• thromboxane
• tissue

• Youville Research Institute, St. Boniface General Hospital, and Faculty of Medicine, University of Manitoba, Winnipeg, Canada

  Naranjan S. Dhalla, Ian R. Innes, Robert E. Beamish

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