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Current evidence suggests that the ischemic preconditioning response is a multi-factorial process consisting of an initial early trigger, an intermediate mediator, and an end effector. Each of these steps in is now its own intense area of investigation. The need to render the heart ischemic for a brief period to invoke the preconditioning response is currently the major factor limiting clinical application of this powerful cardioprotective strategy. Recent research efforts have utilized brief exposures to pharmacological agents, in lieu of a brief preconditioning ischemia, to trigger/mimic the ischemic preconditioning-induced response. The World Heart Congress held in Winnipeg in July 2001 provided a forum for the presentation of new insights into the basic mechanisms of ischemia and reperfusion injury, as well as novel strategies to protect the heart from cell death, ventricular arrhythmias, and contractile dysfunction. Many pioneers in the fields of ischemia-reperfusion injury and preconditioning-induced protection presented there and the chapters in this book represent selected papers from these symposia.
Table des matières
Dedication: A Tribute to Dr. Lionel Opie. Preface. Acknowledgments. I: Ischemia/Reperfusion Injury: Basic Mechanisms. 1. PTCA Acutely Expands Perfused Myocardial Mass and Increases Flow Homogeneity; G. Sambuceti, et al. 2. Angiogenic Therapy by Coronary Collateral Recruitment and Arteriogenesis; M. Fujita. 3. Regulatory Role of ERK-Dependent Pathways in Activity of the Na+/H+ Exchanger in the Healthy and Ischemic Myocardium; L. Fliegel, et al. 4. Sodium Overload and Mitochondrial Damage in Inschemic/Reperfused Heart; S. Takeo, et al. 5. Antisense-Induced Underexpression of Manganese Superoxide Dismutase Extends Myocardial Ischemia-Reperfusion Injury; S. Hoshida, et al. 6. Phospholamban Phosphorylation During Ischemia and Reperfusion Injury: Mechanisms and Functional Implications; A. Mattiazzi, et al. 7. Phospholipase C-Mediated Signaling in Ischemic Heart Disease; P.S. Tappia, et al. 8. Effects of Sequential Ischemia-Reperfusion Cycles on Cyclic Nucleotide Phosphodiesterase Activity in Pig Heart; T. Podzuweit, et al. 9. Inducible Nitric Oxide Synthase in Cardiac Adaption to Ischemia; J. Slezak, et al. 10. Long Term Follow-Up of Leukocyte Function During Myocardial Reperfusion Injury; E. Röth, et al. 11. Mechanisms of Cellular Alterations Due to Ischemia-Reperfusion Injury in the Heart; R. Temsah, et al. 12. Mechanisms for Ischemia/Reperfusion Injury: Application of 23Na Magnetic Resonance Spectroscopy; K. Imahashi, H. Kusuoka. II: Mechanisms Underlying Ischemic Preconditioning-Induced Cardiop
Résumé
Current evidence suggests that the ischemic preconditioning response is a multi-factorial process consisting of an initial early trigger, an intermediate mediator, and an end effector. Each of these steps in is now its own intense area of investigation. The need to render the heart ischemic for a brief period to invoke the preconditioning response is currently the major factor limiting clinical application of this powerful cardioprotective strategy. Recent research efforts have utilized brief exposures to pharmacological agents, in lieu of a brief preconditioning ischemia, to trigger/mimic the ischemic preconditioning-induced response. The World Heart Congress held in Winnipeg in July 2001 provided a forum for the presentation of new insights into the basic mechanisms of ischemia and reperfusion injury, as well as novel strategies to protect the heart from cell death, ventricular arrhythmias, and contractile dysfunction. Many pioneers in the fields of ischemia-reperfusion injury and preconditioning-induced protection presented there and the chapters in this book represent selected papers from these symposia.
