β受体阻滞剂对大鼠急性缺血心肌间隙连接蛋白43的影响  

Effects of β-receptor blocker on connexin 43 of myocardial gap junction after acute ischemia injury

作　　者：王电烨[1] 李永慧[1] 李胜建[1] 

机构地区：[1]山西医科大学第二医院,030001

出　　处：《山西医药杂志》2007年第5期410-412,共3页Shanxi Medical Journal

摘　　要：目的观察两种β受体阻滞剂对大鼠急性缺血心肌连接蛋白43(Cx43)的影响,进一步探讨其抗心律失常的可能机制。方法将40只大鼠随机分成假手术组(SM组10只)、缺血组(IM组10只)、美托洛尔组(MTP组10只)和卡维地洛组(CVD组10只)。结扎左冠状动脉前降支致缺血1 h,建立在体急性心肌缺血模型,观察各组心律失常的发生情况;应用免疫组织化学SP法检测Cx43在各组急性缺血心肌中的表达;应用黄嘌呤氧化酶法和硫代巴比妥酸法测各组动物血清中丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活力;应用电镜观察各组心肌超微结构的改变。结果IM组与SM组比较,心律失常评分和血清MDA含量显著增高,SOD活力降低,心室肌Cx43含量显著降低、分布紊乱;与IM组相比,MTP、CVD组心律失常评分显著降低,Cx43含量增高、分布规律;CVD组与MTP组相比,心律失常评分和血清MDA含量降低,SOD活力增高,Cx43含量增高、分布较均一。结论β受体阻滞剂能有效抑制急性心肌缺血心室肌Cx43降解,减少心律失常的发生,其中卡维地洛作用较强,其机制可能与β受体阻滞和抗氧化有关。Objective To observe the effects of β-receptor blocker on connexin 43 in order to make clear the protective mechanism against ischemia-induced arrhythmias. Methods The rats were randomly divided into 4 groups： SM operation group （group SM, n = 10）, ischemia group （group IM, n = 10）, metoprolol group（group MTP, n = 10 ）, carvedilol group（group CVD, n = 10）. Myocardial infarction was induced by ligation of the left anterior descending coronary artery for 60 minutes. The expression of connexin 43 of the ischemic myocardium was studied by immunohistochemistry technique. The ventricular arrhythmia was observed and MDA, SOD were measured. The tissue samples of the infarcted areas were examined by electron microscope. Results Carvedilol tablets obviously decreased the VAS caused by ischemia, increased the activity of SOD, inhibited the reduction of MDA content in serum, and resulted in normal distribution and composition of Cx43 compared with IM and MTP group. Conclusion β-receptor blocker can effectively alleviate Cx43 degrading induced by acute myocardial infarction, Carvedilol is comparatively more effective among the total, Mechanism of this effect is associated with resisting oxidative stress and β-receptor blockage.

关 键 词：连接蛋白43 心律失常 Β受体阻滞剂 心肌缺血 

分 类 号：R541[医药卫生—心血管疾病]