线粒体ATP敏感性钾通道开放剂二氮嗪对大鼠缺血心肌细胞的保护作用

Cardioprotective effects of Mitochondrial ATP-sensitive potassium channel opener diazoxide on ischemic myocardial cells

目的评价线粒体ATP敏感性钾通道(mitoKATP)开放剂二氮嗪对缺血损伤的心肌细胞超微结构和死亡率的影响。方法选用Wistar大鼠30只,随机分为正常对照组、心肌细胞损伤模型组(皮下注射异丙肾上腺素5mg/kg)和二氮嗪20mg/kg组。24h后处死动物,观察心肌细胞超微结构的改变。结果异丙肾上腺素皮下注射可以引起心肌细胞超微结构明显受损,预先给予二氮嗪口服可以减轻超微结构的损伤。二氮嗪10～100μmol/L可以降低缺血心肌细胞的死亡率,与对照组比较差异有统计学意义(P<0.01)。结论二氮嗪对缺血损伤的心肌细胞具有保护作用。

Objective To evaluate the effects of mitochondrial ATP-sensitive potassium channel opener diazoxide on ultrastructural changes in myocardial cells and myocyte mortality in isoproterenol-induced myocardial ischemic rats. Methods Thirty Wistar rats were randomly divided into 3 groups： control group, myocardial ischemic group （with 5 mg/kg isoproterenol injection subcutaneously） and experimental group （20 mg/kg diazoxide injection before the ischemic injure）. Results Isoproterenol injection could damage the myocardial cell ultrastructures, which could be mitigated by preconditioning diazoxide injection. 10-100 μmol/1 diazoxide could significantly decrease the mortality of ischemic myocardial cells compared to the control group （P〈 0.01）. Conclusions Mitochondrial ATP-sensitive potassium channel opener diazoxide has a cardioprotective effect on myocardial ischemia.