mitoK_(ATP)通道参与心肌缺血预处理保护作用的机制  

MECHANISMS OF CARDIOPROTECTION INDUCED BY PRECONDITIONING AFTER ACTIVATION OFMITOK ATP CHANNEL

作　　者：张蓓[1] 汤伯瑜[1] 张红[1] 朱立[2] 陈莹莹[2] 沈岳良[2] 

机构地区：[1]湖州师范学院,浙江湖州313000 [2]浙江大学医学院生理教研室,浙江杭州310058

出　　处：《中国应用生理学杂志》2007年第2期190-193,共4页Chinese Journal of Applied Physiology

基　　金：湖州市社会发展科技计划资助项目(2004YS18)

摘　　要：目的探讨血管紧张素转换酶抑制剂(ACEI)和阈下缺血预处理联合预处理诱导的心肌保护作用中mi-toK_(ATP)通道激动后的作用机制。方法采用离体大鼠心脏Langendorff灌流模型,观察心脏电脱耦联发生时间、细胞膜Na+/K+-ATPase和Ca2+/Mg2+-ATPase活性的改变。结果单独使用卡托普利、或给予大鼠心脏2min缺血/10min复灌作为阈下缺血预处理,均不能改善长时间缺血/复灌引起的心脏收缩功能下降。而卡托普利和阈下缺血预处理联合使用可增高心脏收缩功能。mitoK_(ATP)通道特异性阻断剂5-HD可取消这一联合预处理的作用。联合预处理可引起缺血后电脱耦联发生时间延长,缺血心肌细胞膜Na+/K+-ATPase和Ca2+/Mg2+-ATPase活性增高;5-HD可取消此作用。结论mitoK_(ATP)通道参与了联合预处理延迟缺血引起的细胞间脱耦联和促进细胞膜离子通道稳定性维持的作用。To determine mechanisms of cardioprotection induced by combination angiotensin-converting enzyme inhibitors（ ACEI ） with subthreshold preconditioning after activation of mitochondrial ATP-sensitive potassium（mitoKaTp）channd. Methods： The Lan-gendorff model of isolated rat heart was used. The time of the onset of uncoupling, the activities of sarcolemmal Na^＋/K^＋-ATPase and Ca^2＋/Mg^2＋-ATPase were measured. Results： The subthreshold preconditioning （2 min of ischemia and 10 min reperfusion） or captopril（an ACEI） alone did not protect hearts against injury of sustained ischemia. However combination eaptopril with subthresh-old preconditioning increased L VDP. Pretreatment hearts with mitoKaTP channel inhibitor 5-HD abolished the protection effect. Combination eaptopril with subthreshold preconditioning delayed the onset of uncoupling, and enhanced the activities of sarcolemmal Na^＋/K^＋-ATPase and Ca^2＋/Mg^2＋-ATPase in ischemia/reperfusion hearts. But 5-HD cancdled these cardioprotection effects. Con- clusion： Combination ACEI with subthreshold preconditioning delays the onset of cellular uncoupling induced by acute ischemia, and promotes the stability of sarcolemmal ion channels, in which activation of the mitoKaTP channels may be involved.

关 键 词：血管紧张素转换酶抑制剂 阈下缺血预处理 线粒体ATP敏感性钾通道 脱耦联 

分 类 号：Q463[生物学—生理学]