Myocardial Ischemia and Preconditioning, 2003 Progress in Experimental Cardiology Series, Vol. 6

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.

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-InducedCardioprotection. 13. Is Reduced Cell Swelling a Plausible End-Effector of Ischemic Preconditioning Protection? C.E. Ganote, et al. 14. Cardioprotection by Mitochondrial KATP Channel in Both Early and Late Preconditioning; Yigang Wang, et al. 15. Role of Mitochondrial Membrane Potential in Cardiac Protection Against Ischemia; Meifeng Xu, et al. 16. Hypoxic Reperfusion After Brief Ischemia Potentiates Ischemic Preconditioning in Isolated Rat Hearts; M.-C. Toufektsian, et al. 17. Molecular Basis for the Cardioprotective Effect of Herbal Drugs in Ischemic Heart Disease: An Experimental Study; S.K. Gupta, et al. 18. Ischaemic and Pharmacological Preconditioning is Associated with Attenuation of p38 MAPK Activation During Sustained Ischaemia and Reperfusion; A. Lochner, et al. 19. A Role for the Phosphatidylinositol-3-Kinase Pathway in Preconditioning; E. Murphy, et al. 20. Myofilament Calcium Responsiveness in Stunning and Preconditioning; N.G. Pérez. 21. How to Mediate Cardioprotection in Ischemic Hearts &endash; Role of Adenosine; M. Kitakaze. 22. On the Role of Adenosine in Classical and Interorgan Preconditioning of the Heart; D.A. Liem, et al. 23. Adenosine A3 Receptor Induced Delayed Preconditioning: Essential Role of Nuclear Factor κB, Nitric Oxide Synthase and Mitochondrial KATP Channels; T.C. Zhao, R.C. Kukreja. 24. Activation of Adenosine A1 and A3 Receptors Protects Mitochondria During Hypoxia in Cardiomyocytes by Distinct Mechanisms; V. Shneyvays, et al. 25. Non Ischemic Myocardial Preconditioning b