Review article
Reperfusion injury

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Abstract

Several lines of evidence point to a major role of oxygen free radicals in the pathogenesis of cell death or dysfunction in a variety of disease processes. Recent studies from this as well as other laboratories have demonstrated that oxygen free radicals play a major role in the pathogenesis of post-ischemic reperfusion injury in the heart.1–4 We have recently developed methods for direct measurement of radical species and/or specific byproducts of radical injury.5 Timely administration of oxygen radical scavengers reduced the quantity of free radicals generated following reperfusion and in addition improved recovery of post-ischemic ventricular function and metabolism.3,6 In a regionally ischemic model the free radical scavenger recombinant human superoxide dismutase also administered at the time of reflow was shown to limit infarct size.4 In this article we review the biophysical and molecular mechanisms of oxygen free radical generation that are viewed as contributing to post-ischemic reperfusion injury. We also discuss the mechanisms by which the body defends against free radical attack and the interrelationship of free radical injury to other mechanisms of tissue injury.

Keywords

Myocardial reperfusion injury
Oxygen free radicals
Superoxide radicals
Hydroxyl radicals
Free radical scavengers
Superoxide dismutase

Cited by (0)

John T. Flaherty received his B.S. degree in Engineering from the Massachusetts Institute of Technology in 1963 and his M.D. degree from Duke University School of Medicine in 1967. He did his training in Internal Medicine and in Cardiology at the Johns Hopkins Hospital between 1967 and 1974. During that time he also spent 3 years as a Research Fellow at the National Heart Institute. Dr. Flaherty joined the faculty of the Cardiology Division at the Johns Hopkins University School of Medicine in 1974 and is currently Associate Professor of Medicine. Dr. Flaherty has a longterm research interest in the pathophysiology of ischemic myocardial injury. He is the author of more than 100 journal articles and book chapters dealing with protection of ischemic myocardium and more recently with studies of reperfusion injury.

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Myron L. Weisfeldt, M.D., is a Professor of Medicine and has been the Director of Cardiology at Johns Hopkins Medical Institutions since 1975. Dr. Weisfeldt is the Director of the Ischemic Heart Disease Specialized Center of Research Program from the National Heart, Lung and Blood Institute since 1978. He is currently President-Elect of the American Heart Association, and is Chairman of the NHLBI Cardiology Advisory Committee. Also he is on the Editorial Board of Circulation, Circulation Research and the Journal of Molecular and Cellular Cardiology. His research interests include mechanisms of ischemic injury, age changes in cardiac function and cardiopulmonary resuscitation. He has served on the national AHA Committees dealing with CPR standards.