Reactive oxygen species may cause myocardial reperfusion injury.
The pathogenic mechanisms responsible for heart damage following temporary coronary artery occlusion are unknown. Some damage may be mediated by a normal cellular enzyme, xanthine dehydrogenase, which converts to xanthine oxidase during myocardial ischemia. Reperfusion, with restoration of oxygen supply, may then lead to formation of superoxide by xanthine oxidase, possibly initiating a cascade of oxidative events. In support of this, reperfusion of transiently ischemic canine myocardium leads to a rapid loss of cellular glutathione and a decrease in catalase activity, both indicative of enhanced generation of activated oxygen. Allopurinol--an inhibitor of xanthine oxidase--ameliorates both biochemical damage and functional deficits ordinarily triggered by ischemia and reperfusion, suggesting one possible mode of pharmacologic intervention following acute myocardial infarction.
D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D002374:Catalase / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D005978:Glutathione / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D010477:Perfusion; D013997:Time Factors; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors
D000493:Allopurinol; D002374:Catalase; D014969:Xanthine Oxidase; D005978:Glutathione; D010100:Oxygen