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目的:探讨美托洛尔对大鼠心肌梗死(心梗)后梗死周边区缝隙连接蛋白43(Cx43)的影响。方法:80只大鼠随机分为假手术组(20只)、心梗组(30只)和美托洛尔组(30只),用结扎冠状动脉左前降支的方法制备心梗模型,美托洛尔组给予美托洛尔5mg/(kg.d)灌胃,心梗组给予安慰剂。手术8周后,测量梗死周边区心室颤动阈值(室颤阈值)。用蛋白印记分析和RT-PCR分别观察心梗后梗死周边区缝隙连接蛋白43(Cx43)磷酸化的蛋白质及总量表达和mRNA表达的变化;免疫荧光法观察梗死周边区Cx43的分布。结果:8周后,美托洛尔组室颤阈值高于心梗组[(11.0±2.65)V比(7.1±4.1)V,P<0.05],美托洛尔组Cx43磷酸化的蛋白质及总量均显著高于心梗组,Cx43mRNA的表达也明显高于心梗组。Cx43的密度和分布均显著高于心梗组。结论:美托洛尔能显著改善梗死周边区缝隙连接重构,这可能是美托洛尔能够抑制心梗后室性心律失常的一个机制。
Objective: To investigate the effect of metoprolol on connexin43 (Cx43) in peripheral infarction area after myocardial infarction in rats. Methods: Eighty rats were randomly divided into sham operation group (20 rats), myocardial infarction group (30 rats) and metoprolol group (30 rats). Myocardial infarction model was made by ligation of the left anterior descending coronary artery Metoprolol was given orally to metoprolol 5 mg / (kg.d), and placebo was given to the MI group. After 8 weeks of surgery, the ventricular fibrillation threshold (ventricular fibrillation threshold) was measured in the peripheral infarct area. Western blot analysis and RT-PCR were used to observe the changes of Cx43 protein expression and mRNA expression in infarcted peripheral area respectively. The distribution of Cx43 in the peripheral infarction area was observed by immunofluorescence. Results: After 8 weeks, the threshold of ventricular fibrillation in metoprolol group was higher than that in myocardial infarction group [(11.0 ± 2.65) V vs (7.1 ± 4.1) V, P <0.05]. The phosphorylated Cx43 protein in metoprolol group and The total amount was significantly higher than the myocardial infarction group, the expression of Cx43 mRNA was also significantly higher than the myocardial infarction group. The density and distribution of Cx43 were significantly higher than the myocardial infarction group. Conclusion: Metoprolol can significantly improve the peri-infarct junctional remodeling, which may be a mechanism by which metoprolol can inhibit ventricular arrhythmia after myocardial infarction.