论文部分内容阅读
冠状动脉损伤对心肌不能供应动脉血时可使心功能下降,继而导致心肌细胞坏死。对这种缺血性心脏病病因的探讨一向是从心肌供氧不足引起能量缺乏为主的代谢方面进行研究。因而,一般认为随缺血所致糖酵解系统亢进而产生以乳酸为代表的最终代谢产物蓄积可使心肌细胞内pH下降,同时又是损害心肌细胞功能的主要原因。然而另一方面已知,①在缺血心肌儿茶酚胺的游离增加,②随心肌酸中毒,ATP分解为次亚黄嘌呤,③黄嘌呤脱氢酶(XD)在血管内皮细胞内转化为黄嘌呤氧化酶(XO)即D→O转化,④环氧化酶被激活等。在厌氧条件下,这些代谢性变化通过儿茶酚胺的自动氧化和以黄嘌吟为底物的黄嘌呤氧化酶反应以及前列腺素G_2(PGG_2)转化为前列腺素H_2(PCH_2)等提供了
Coronary artery injury can not supply the heart muscle can make the heart function decline, and then lead to myocardial necrosis. The etiology of this ischemic heart disease has always been to study the metabolic aspects of the lack of oxygen due to lack of energy caused by myocardial ischemia. Therefore, it is generally believed that the accumulation of the final metabolites such as lactate caused by the hyperactivity of the glycolysis system caused by ischemia may decrease the intracellular pH and at the same time is the main reason for impairing cardiomyocyte function. On the other hand, however, it has been known that ① free dissociation of catecholamines in the ischemic myocardium, ② decomposition of ATP to hypoxanthine due to cardiac acidosis, and xanthine dehydrogenase (XD) into xanthine oxidation in vascular endothelial cells Enzyme (XO) D → O conversion, ④ cyclooxygenase is activated and so on. Under anaerobic conditions, these metabolic changes are provided by the auto-oxidation of catecholamines and the xanthine oxidase reaction with xanthine as substrate and the conversion of PGG_2 to PCH_2