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目的 :探讨维拉帕米对缺血再灌注损伤心肌的保护作用及其机制。方法 :①建立家兔心肌缺血再灌注模型。将 2 4只家兔按再灌注时限的不同及是否给予维拉帕米 (0 .2mg/kg静脉注射 )干预分为 4组 (A1、A2、B1、B2 ) ,测定各组的心肌梗死范围 ,并在电镜下对缺血再灌注心肌进行超微结构观察。②根据心肌缺血再灌注不同时限对 33只家兔进行分组 ,采用免疫组化法检测同一剂量维拉帕米 (0 .2mg/kg静脉注射 )对缺血再灌注不同时限心肌组织bcl 2蛋白的表达情况。结果 :①与 0 .85 %氯化钠组比较 ,维拉帕米组可明显减小心肌梗死范围(P <0 .0 1) ,改善其超微结构的变化。②与假手术对照组和 0 .85 %氯化钠组比较 ,维拉帕米组能显著上调缺血再灌注心肌bcl 2蛋白的表达 (P <0 .0 1)。结论 :维拉帕米可明显减轻心肌缺血再灌注损伤 ,其心肌保护机制可能是通过其促进缺血再灌注心肌组织bcl 2蛋白的表达来实现的
Objective: To investigate the protective effect of verapamil on myocardial ischemia-reperfusion injury and its mechanism. Methods: ① To establish rabbit myocardial ischemia-reperfusion model. 24 rabbits were divided into 4 groups (A1, A2, B1 and B2) according to the reperfusion time limit and verapamil (0.2 mg / kg intravenous injection), and the myocardial infarct size , And the ultrastructure of ischemia-reperfusion myocardium was observed under electron microscope. (2) 33 rabbits were divided into groups according to the different time points of myocardial ischemia-reperfusion, and the same dose of verapamil (0.2 mg / kg) was used to detect the expression of bcl 2 protein The expression of the situation. Results: ①Compared with 0.85% sodium chloride group, the verapamil group could significantly reduce the range of myocardial infarction (P <0.01) and improve the ultrastructure of myocardium. ② Compared with the sham operation control group and the 0.85% sodium chloride group, the verapamil group could significantly up-regulate the expression of bcl 2 protein (P <0.01). Conclusion: Verapamil can significantly reduce myocardial ischemia-reperfusion injury, and its myocardial protective mechanism may be through its promotion of ischemia-reperfusion myocardial bcl 2 protein expression to achieve