M3受体在脑心综合征心律失常中的作用

Role of ventricular M_3 receptor in arrhythmia resulted from cerebral-cardiac syndrome

观察M3受体(M3R)在脑心综合征(CCS)模型大鼠心室肌中的作用及其表达,以探讨其与CCS心律失常的关系。线栓法建立CCS模型,监测心电图,激光共聚焦扫描显微镜记录激动M3R后心肌细胞内钙的变化,Western blotting检测心室肌中M3R表达水平的改变。同对照组相比,模型组心电图QRS、QT间期显著延长(P<0.01);Western blotting结果显示模型组心室肌中M3R的表达水平较对照组显著降低(P<0.05);胆碱激动M3R可以抑制KCl除极诱导的模型组心肌细胞内钙的升高幅度(P<0.01),其特异阻断剂4-DAMP可以阻断这一作用。M3R表达降低可能是CCS心律失常的重要原因之一。激动M3R可以降低心肌细胞内钙,M3R可能是治疗CCS心律失常新的靶点。

To detect the function and expression of ventricular M3 receptor （M3 R） in cerebral-cardiac syndrome （CCS） model rats and to explore the relationship between the expression of M3R and the arrhythmia resulted from CCS, CCS model rats were induced by occluding right middle cerebral artery. ECG was monitored. Intracellular calcium （ [ Ca^2＋ ]i） changes after agitating M3R were recorded by laser scanning confocal microscope. Changes of M3R expression in the ventricular tissue were detected by Western blotting. QRS and QT intervals in CCS group were remarkably longer than that in sham group. According to the results of Western blotting, the level of M3R expression was remarkably lower in CCS group compared with that in the normal group. KCl induced [ Ca^2＋ ]i increasing in CCS group could be depressed by choline and the effect of choline could be blocked by 4-DAMP. The lower expression of M3R in CCS group may be one of important reasons of arrhythmia resulted from CCS. M3 R that depressed the [ Ca^2＋ ]i increasing agitated by choline may become a new target to cure arrhythmia resulted from CCS.