预处理减轻器官缺血再灌注损伤机制的研究进展及应用前景  

Progress of the preconditioning mechanism on ischemia-reperfusion injury and its application prospect

作　　者：王姗姗[1] 韩如泉[1] 

机构地区：[1]首都医科大学附属北京天坛医院麻醉科,北京100050

出　　处：《首都医科大学学报》2013年第6期910-914,共5页Journal of Capital Medical University

基　　金：高层次卫生技术人才队伍建设工程(2009-3-19)~~

摘　　要：缺血性疾病是临床中常见的一种病理生理过程,一旦发生在心脑等重要器官可能导致严重后果。缺血后再灌注能明显减少组织器官梗死面积,但同时可能造成缺血再灌注损伤。大量研究显示预处理对缺血再灌注损伤有强大的保护作用。预处理保护缺血再灌注损伤的机制包括:减少氧化应激反应,抑制活性氧(reactive oxygen species,ROS)及一氧化氮(nitric oxide,NO)释放,抑制胞内钙离子超载,激活线粒体ATP依赖性钾离子通道,减轻炎性发应等来减少组织细胞死亡以实现对器官缺血再灌注损伤的保护作用。本文就预处理对缺血/再灌注损伤的保护机制及其应用前景进行综述。Ischemic disease is a common pathophysiological phenomenon which might cause serious complications when occurred in the vital organs such as heart and brain. Reperfusion can significantly reduce infarct size, but may result in ischemia-reperfusion injury at the same time. Numerous studies have shown that preconditioning is a powerful intervention to alleviate ischemia/reperfusion injury . The mechanisms include suppression of oxidative stress response, inhibition of reactive oxygen species（ROS） and nitric oxide （NO） release, reduction of intraceltular calcium overload, activation of mitochondrial ATP-sensitive potassium chanels , and decreasing inflammation response. In this paper, the preventive effect and mechanism of preconditioning on ischemia/reperfusion injury were reviewed.

关 键 词：缺血再灌注损伤 预处理 氧化应激 钙离子超载 炎性反应 

分 类 号：R743.31[医药卫生—神经病学与精神病学]