Reperfusion injury of postischemic tissues.
Reperfusion injury, occurring when blood circulation is restored to previously ischemic tissues, is now demonstrable as a pathophysiologic entity distinct from the primary ischemic injury that develops during ischemia per se. The primary pathogens that cause reperfusion injury are thought to be partially reduced oxygen species, including superoxide radicals, hydrogen peroxide, and hydroxyl radicals, which initiate lipid peroxidation and other deleterious oxidation reactions during the reperfusion period. Antioxidant drugs, given at the end of ischemia or at the very onset of reperfusion, can improve the postischemic function of isolated organs and the survival of intact animals subject to a cycle of circulatory arrest and reperfusion, suggesting that reperfusion injury is both a real and a preventable pathophysiologic entity.
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Hillenbrand Biomedical Engineering Center, Purdue University, West Lafayette, Indiana 47907.
D000818:Animals; D005609:Free Radicals; D006801:Humans; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology
D005609:Free Radicals