冠脑益嗪对大鼠心肌缺血/再灌注损伤保护作用的机制

目的 :观察冠脑益嗪对大鼠心肌缺血 /再灌注损伤的影响 ,探讨其保护作用的机制。方法 :采用在体大鼠心肌缺血 /再灌注模型 ,于结扎冠状动脉前 3m in iv冠脑益嗪 ,观察在心肌缺血 /再灌注状态下心电图、心肌丙二醛（MDA）、超氧化物歧化酶 （SOD）、Ca2 +、游离脂肪酸 （FFA）及血清中肌酸激酶 （CK）、乳酸脱氢酶 （L DH）的变化。结果 :冠脑益嗪能显著降低缺血 /再灌注损伤引起的室性心律失常发生率 ,缩短持续时间 ;升高 SOD活性 ,减少 MDA生成 ;减少 Ca2 +在心肌组织内的聚积 ;亦能明显降低心肌 CK、L DH和 FFA的释放。结论 :冠脑益嗪对大鼠心肌缺血 /再灌注损伤的保护作用可能与保护氧自由基清除酶的活性 ,防止膜脂质过氧化及阻断钙内流有关

Protective effect of corocinnarine on ischemia-reperfusion myocardium of rats and its relation to anti-lipid peroxidation

AIM: To study the protective effect of corocinnarine (Cor) on ischemia-reperfusion myocardium. :The myocardial ischemia-reperfusion model of rats in vivo was applied to the present study. Cor (5.0 mg kga-1)was injected intravenously 3 min before the ligation of coronary artery. ECGs of rats under ischemia-reperfusion condition were recorded. The contents of myocardial malondialdehyde (MDA), superoxide dismutase (SOD), calcium, myocardial creatine kinase (CK) and lactate dehydrogenase (LDH) in serum were measured.: Pretreatment with Cor could significantly decrease the incidence and duration of ventricular arrhythmias induced by myocardial ischemia-reperfusion, reduce the release of myocrdial CK and LDH, lower the calcium accumulation in myocardium, decrease the generation of MDA and improve the activity of SOD.:Cor has a significant protective effect on myocardial ischemia-reperfusion injury and the protective effect might associate with its effects of improving SOD activity and prohibiting lipid peroxidation.