心肌缝隙连接在缺血预适应中的作用  

作　　者：苏德淳[1] 常志文[1] 

机构地区：[1]首都医科大学附属北京同仁医院,北京100730

出　　处：《山东医药》2006年第13期9-11,共3页Shandong Medical Journal

基　　金：北京市教育委员会科技发展计划资助项目(KM200610025026)

摘　　要：目的探讨心肌缝隙连接(GJ)在缺血预适应(IPC)心肌保护中的地位和作用。方法将72只大鼠分为缺血再灌注组(对照组)、IPC组、IPC+5-羟基奎酸(5-HD)组、二氮嗪(Dia)组、Dia+5-HD组、甘草次酸(GA)组、GA+5-HD组、GA+IPC组,测量各组的血流动力学指标、心肌梗死面积和心律失常发生情况。结果与对照组相比,IPC组、Dia组、GA组能降低心肌梗死面积,减少心律失常;5-HD能阻断IPC和Dia的心肌保护作用,对GA无影响。IPC加用GA不能抑制IPC的保护作用。结论在IPC信号传导通路中,GJ位于线粒体ATP敏感性钾通道的下游,可能是IPC的终末效应器,但在IPC触发阶段不起作用。Objective, To explore the importance and effects of myocardial gap junction （GJ） on cardioprotection in ischemic preconditioning （IPC）. Methods： Seventy-two rats were randomly divided into 8 groups： ischemia-reperfusion （control）, IPC, IPC＋5-hydroxydecanoic acid （IPC＋5-HD）, diazoxide （Dia）, Dia ＋ 5-HD, 18β-glycyrrhetinic acid （GA）, GA＋ 5-HD, and GA＋IPC. Hemodynamics, myocardial infarct area and incidence of arrhythmia were determined in all groups. Results： IPC, Dia, and GA reduced infarct area and incidence of arrhythmia compared with the control group. 5-HD blocked the cardioprotection of preconditioning and diazoxide, but had no effects on GA. Additional GA didn＇t affect the cardioprotection in IPC. Conclusions： Gap junction is downstream of mitochondrial ATP sensitive potassium channel in the signaling pathway of IPC and is the end effectors of IPC, but it has no effects during trigger phase of IPC.

关 键 词：缝隙接合部 缺血预处理 心肌 心肌梗死 心律失常 心肌保护 

分 类 号：R542.2[医药卫生—心血管疾病]