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临床采用扩张血管、溶栓、抗凝以及血管搭桥等方法治疗心肌梗塞和脑梗塞等血管闭塞性疾病时,发现许多病人病情反而加重、恶化。研究证 实这主要是由于不恰当的再灌注所引起,其发生机制包括钙离子超载、花生四烯酸及其代谢产物的生成以及自由基连锁反应等,它们相互协同,最终导致细胞的不可逆损害。本文就组织缺血后不恰当再灌注后引起自由基连锁反应的机制及其损害作用做一讨论。 正常情况下,机体内产生自由基和清除自由基(FR)系统处于动态平衡,故存在的自由基不至于引起机体损害。在组织缺血缺氧时,氧供下降,三磷酸腺苷(ATP)减少,细胞正常代谢途径受到破坏。由于能量衰竭,使慢钙通道开放,钙离子(Ca~(2+))内流增加。
Clinical use of dilation of blood vessels, thrombolysis, anticoagulation and vascular bypass and other methods of treatment of vascular occlusive disease such as myocardial infarction and cerebral infarction, found that many patients rather aggravate the disease. Studies have confirmed that this is mainly due to inappropriate reperfusion caused by the mechanism of calcium overload, arachidonic acid and its metabolites and free radical chain reaction, etc., they cooperate with each other, eventually leading to irreversible damage to cells. This article discusses the mechanism of the free radical chain reaction caused by inappropriate ischemia after tissue ischemia and its damage. Under normal circumstances, the body produces free radicals and free radical scavenging (FR) system in a dynamic equilibrium, so the existence of free radicals will not cause damage to the body. In tissue ischemia and hypoxia, oxygen supply decreased, adenosine triphosphate (ATP) decreased, the normal metabolic pathway of cells destroyed. Due to energy failure, so that slow calcium channels open, calcium (Ca ~ (2 +)) influx increased.