摘要
目的探讨心肌缺血时,心肌缝隙连接蛋白43(connexin43,Cx43)与缺血性心律失常的关系。方法对戊巴比妥钠麻醉大鼠进行30min的冠状动脉缺血。大鼠分为不处理或者接受缺血预适应(ischemic preconditioning,IPC)、静脉注射线粒体ATP磷酸敏感性钾通道(mitoKATP)开放剂二氮嗪(Dia)3组,其余2组为在接受IPC、Dia的基础上加用5羟基奎酸(5-HD)。测量各组的血流动力学指标和心律失常。采用Western blotting检测Cx43的磷酸化程度。结果与对照组相比,IPC、Dia能促进Cx43磷酸化,减少心律失常的发生率,线粒体ATP敏感性钾通道阻断剂5-HD能消除IPC和Dia的上述作用。结论IPC通过开放线粒体ATP敏感性钾通道促进Cx43磷酸化和电耦联,进而抑制心律失常的发生。
Objective To explore the relationship between connexin43 and ischemic arrhythmia during myocardial ischemia. Methods Barbiturate-anesthetized rats were subjected to a 30 min coronary artery occlusion. Rats were randomly assigned to control or ischemic preconditioning, and diazoxide groups. In two additional groups, rats received 5-hydroxydecanoic acid in the presence of ischemic preconditioning or diazoxide. Hemodynamics and arrhythmia were determined. Changes in phosphorylation of connexin43 were defined with quantitative immunoblotting. Results Ischemic preconditioning and diazoxide, a mitochondrial ATP sensitive potassium channel agonist induced phosphorylation of connexin43 and reduced arrhythmias as compared to control groups. The ATP sensitive potassium channel blocker 5-hydroxydecanoic acid prevented these effects in preconditioned and diazoxide hearts. Conclusion Ischemic preconditioning induces phosphorylation of connexin43 and electrical coupling by opening mitochondrial ATP sensitive potassium channel and then prevents the development of arrhythmias.
出处
《首都医科大学学报》
CAS
2006年第3期325-328,共4页
Journal of Capital Medical University
基金
北京市教委科技发展基金(KM200610025026)资助项目
关键词
缝隙连接
缺血预适应
心肌
心律失常
gap junction
ischemic preconditioning
cardiac muscle
arrhythmia
