中国胸心血管外科临床杂志

中国胸心血管外科临床杂志

二氮嗪预处理对大鼠心肌缺血-再灌注损伤的保护作用

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目的观察二氮嗪预处理对在体大鼠心肌缺血-再灌注损伤的保护效果,并对其作用机制进行初步的探讨。方法健康SD大鼠14只,采用随机数余数分组法分为两组,对照组和二氮嗪预处理组,每组7只。二氮嗪预处理组按12.5mg/kg的剂量静脉注射二氮嗪溶液,对照组在心肌缺血前静脉注射等量溶媒溶液,结扎冠状动脉前降支致缺血2h,再灌注2h后取心脏,检测缺血心肌组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、心肌梗死面积,观察缺血区凋亡心肌细胞和心肌细胞超微结构的改变。结果二氮嗪预处理组缺血心肌组织MDA含量、心肌梗死区占缺血区的重量百分比和心肌细胞凋亡率明显低于对照组(P〈0.05,0.01),心肌超微结构损伤明显轻于对照组。结论二氮嗪预处理对在体大鼠心肌缺血-再灌注损伤具有较好的保护作用。

Objective To observe the protective effects of diazoxide-preconditioning on myocardial ischemiareperfusion injury of rats and discuss its possible mechanisms. Methods Fourteen healthy SD rats were randomly divided into two groups(7 each group),In diazoxide-preconditioning group diazoxide was injected with the dosage of 12.5mg/kg through the vein,and in control group the media with the same amount was only given before ischemia. The left anterior descending branch was ligated for 2 hours. The heart was quickly excised after 2 hours reperfusion to be used for measurement of the quantity of malondialdehyde(MDA), the activity of superoxide dismutase (SOD), the size of myocardial infarct area, and the cell apoptosis and ultrastructure in ischemic area. Results Compared with the control group, the quantity of MDA,the percentage of the weight of myocardial infarct area/ischemic area, and the rate of cell apoptosis in the diazoxide-preconditioning group were greatly reduced (P〈0.05, 0. 01). The damage of cell uhrastructure was obviously alleviated,Conclusion Diazoxide-preconditioning provides evident cardioprotective effect on the myocardial ischemia-reperfusion injury of rats.

关键词: 二氮嗪 心肌保护 缺血-再灌注损伤 凋亡

Key words: Diazoxide; Myocardial protection; Ischemia-reperfusion injury; Apoptosis

引用本文: 赵静,张凯伦,胡志伟. 二氮嗪预处理对大鼠心肌缺血-再灌注损伤的保护作用. 中国胸心血管外科临床杂志, 2005, 12(4): 270-273. doi: 复制

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