ABSTRACT
Damage and Dysfunction ...............................................................................42 3.3 Oxidative and Nitrosative Stress and PARP Activation in Myocardial
Ischemia and Reperfusion ..............................................................................43 3.4 PARP Activation and Energy Substrate Metabolism during
Myocardial Ischemia and Reperfusion: The Role of Mitochondria..............46 3.5 PARP Activation and Leukocyte-Endothelial Interactions during
Myocardial Ischemia and Reperfusion: The Role of Adhesion Molecules........................................................................................................51
3.6 Conclusion ......................................................................................................54 Acknowledgment .....................................................................................................56 References................................................................................................................56
In clinical therapy of acute myocardial infarction, coronary reperfusion has proved to be the only way to limit infarct size by restoring the fractional uptake of oxygen in the heart to maintain the rate of cellular oxidation. However, restoration of flow is accompanied by detrimental manifestations known as “reperfusion injury,” thus directly influencing the degree of recovery.
