附註:Includes bibliographical references and index.
Front Cover -- Inside Cover -- Copyright -- Table of Contents -- Editors / Contributors -- Preface -- Chapter 1: Stress Proteins in Myocardial Protection -- Chaper 2: Heat Stress Proteins: A Possible Route to Myocardial Protection -- Chapter 3: Cardioprotection by Stress Proteins -- Chapter 4: Role of Heat Shock Proteins, Protein Kinase C and ATP-Sensitive Potassium Channel in Delayed Myocardial Protection -- Chapter 5: Hsp70 and Ischemia Tolerance in the Compromised Heart.
Chapter 6: Hsp72 in the Regulation of TNF- Production: Mechanistic Implication of Protection Against Postischemic Myocardial Dysfunction -- Chapter 7: Preconditioning of Cardiac Myocytes: Studies Using Cultured Neonatal Rat Heart Myocytes and Simulated Ischemia -- Chapter 8: Antisense, Heat Shock Proteins and the Heart -- Chapter 9: Stress Proteins in Myocardial Protection: Culture Shock Protein, Heme Oxygenase-1 (Hsp32), Induced by Sublethal Stresses Protects the Heart Against Oxidative Stress -- Chapter 10: Physiological Role of Heat Shock Protein 27.
Chapter 11: Ischemia/Reperfusion Injury and Heat Shock Proteins -- Index.
摘要:Myocardial ischemic syndromes pose a major medical problem and a significant economic health care concern. Reperfusion, although used in the clinical arena as essential to the survival of acutely ischemic heart muscle carries with it the risk of ""reperfusion injury"". Therefore the salvage of additional myocardium is highly desirable. Over a decade ago, it was shown that whole body heat shock activated a powerful endogenous protective mechanism that significantly improved myocardial salvage following prolonged ischemia and reperfusion injury in the heart. A characteristic feature of this heat.
