非心肌组织短暂缺血对心肌保护作用的机制探讨  

The mechanism of myocardial protection by brief ischemia in noncardiac tissue

作　　者：王悦喜[1] 陈运贞[1] 董莉[1] 刘元生[1] 

机构地区：[1]重庆医科大学临床学院心血管内科,重庆 400016

出　　处：《重庆医科大学学报》2000年第4期348-349,共2页Journal of Chongqing Medical University

摘　　要：目的　观察远处其它器官短暂缺血是否能保护心肌及机制的探讨。方法　Wistar大鼠48只,随机分为6组。采用免疫组化方法检测 PKCα、PKCδ亚型在心肌细胞内转移及转位。结果　心肌缺血预处理组（IPC），肠系膜动脉阻塞 （MAO）15min组，股动脉阻塞（FAO）15min组,对心肌都有保护作用。灯盏花素乙(Bre.)不能消除FAO、MAO对心肌的保护作用。免疫组化检测结果除IPC组外,MAO组、FAO组、Bre.干预组心肌细胞内均未见PKCα、PKCδ亚型转位。结论　短暂的肠系膜动脉、 股动脉阻塞和心肌缺血预处理一样能有效保护心肌组织被长时间缺血-再灌注损伤,但其机制与IPC不同,它们并不是经激活PKC信息通道而发挥作用的。： Objective To explore the cardioprotective role and mechanism of brief ischemia in remote organs. Methods 48 Wistar rats were randomly divided into 6 groups. PKCαand PKCδwere measured by immunohistochemistry method. Results 15 minutes occlusion of the mesensteric artery (MAO) and femotall artery (FAO) can protect against myocardial infarction as effectively as coronary artery occlusion (CAO). PKCα and PKCδ did not translocate. Conclusion Brief occlusion of MAO and FAO can protect against myocardial infarction .Their protective mechanism did not pass through the PKC signal passway, which was different from that of myocardiac ischemic preconditioning. The present study may have important clinical implication, because it suggests that ischemia in remote organs can result in cardioprotection when it procedes a coronary thrombotic event.

关 键 词：系膜动脉 心肌缺血 缺血预处理 IPC 心肌保护 

分 类 号：R542.2[医药卫生—心血管疾病]