Peterson D A, Asinger R W, Elsperger K J, Homans D C, Eaton J W
Biochem Biophys Res Commun. 1985 Feb 28;127(1):87-93. doi: 10.1016/s0006-291x(85)80129-7.
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.
暂时冠状动脉闭塞后导致心脏损伤的致病机制尚不清楚。一些损伤可能由一种正常的细胞酶——黄嘌呤脱氢酶介导，该酶在心肌缺血期间会转化为黄嘌呤氧化酶。然后，随着氧气供应的恢复，再灌注可能会导致黄嘌呤氧化酶形成超氧化物，这可能引发一系列氧化事件。支持这一观点的是，短暂缺血犬心肌的再灌注会导致细胞内谷胱甘肽迅速流失以及过氧化氢酶活性降低，这两者都表明活性氧的生成增加。别嘌呤醇——一种黄嘌呤氧化酶抑制剂——可改善通常由缺血和再灌注引发的生化损伤和功能缺陷，这提示了急性心肌梗死后一种可能的药物干预模式。
