Objective To detect the expression and function of ventricular M3 receptor ( M, R) and connexin 43 ( Cx43) in arrhythmia resulted from cerebral-cardiac syndrome ( CCS) model rats. Methods CCS model rats were induced by occluding right middle cerebral artery and electrocardiogram was monitored. The ultrastmcture of the rat myocardium was examined. Changes of M3 R and Cx43 expression in the ventricular tissue were detected by Western blotting. Results The electrocardiogram results showed that QT intervals in CCS model group were remarkably longer than that in control group (P < 0. 01). The electronic microscope results showed that the structure and distribution of ultrastmcture including nucleus, mitochondria, desmosome and gap junction were changed in CCS model group. The Western blotting results showed that the expressions of M3R and Cx43 protein were lower in CCS model 2 hours group than those in control group (P <0.05) ,the expressions of M3R and Cx43 protein were higher in CCS model 24 hours group than those in control group (P<0.05). Conclusion The lower expression of M3 R may be one of important reasons of arrhythmia resulted from CCS, and the effect of arrhythmia may be caused through abnormal expression and distribution of Cx43.%目的 检测M3受体(M3R)及缝隙连接蛋白43( Cx43)在脑心综合征(CCS)模型大鼠心室肌中的表达,并探讨其在脑缺血所致心律失常中的作用.方法 线栓法建立CCS模型,监测心电图;电镜观察心肌细胞的亚显微结构;Western blotting法检测心室肌中M3R和Cx43表达水平的改变.结果 心电图结果显示,与对照组相比,模型组发生心律失常之前的QT间期显著延长(P＜0.01).电镜结果显示,CCS模型组心肌细胞的亚显微结构包括细胞核、线粒体及桥粒和缝隙连接的结构与分布均发生改变.Western blotting结果显示,CCS模型2h组M3R和Cx43与对照组相比显著减少(P＜0.05),CCS模型24h组M3R和Cx43表达增加,且高于对照组(P＜0.05).结论 M3R表达降低可能是CCS心律失常的重要原因之一,其致心律失常的作用可能是通过Cx43表达及分布异常引起的.
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