内皮功能障碍、氧化应激与心肌缺血再灌注损伤  

Oxidative Stress and Endothelial Dysfunction,Myocardial Ischemic Reperfusion Injury

作　　者：连瑞珍[1] 郑玉云[2] 

机构地区：[1]包钢医院心内科,内蒙古包头014010 [2]包头医学院第一附属医院,内蒙古包头014010

出　　处：《疾病监测与控制》2013年第7期416-419,共4页Journal of Diseases Monitor and Control

摘　　要：导致缺血再灌注损伤的机制是多方面的:氧化应激、细胞内钙超载、中性粒细胞活化、血管内皮细胞功能障碍、能量代谢障碍及心肌细胞凋亡等。内皮功能失调是再灌注损伤病理发生的关键。氧衍生自由基明显增加是缺血-再灌注损伤发生的重要机制之一。现就血管内皮细胞功能障碍及氧化应激在心肌缺血再灌注损伤中的作用机制作一综述。Mechanism of ischemia reperfusion injury is multifaceted： oxidative stress, intracellular calcium overload, polymorphonuclear neutrophil activation, endothelial dysfunction, energy metabolism disturbance and cardiomyocyte apoptosis etc. Endothelial dysfunction plays a key role. Oxygenic free radicals increased significantly are one of the important mechanisms of ischemia-reperfusion injury. This review focuses on the mechanisms of endothelial dysfunction and oxidative stress during myocardial ischemia reperfusion injury.

关 键 词：心肌缺血再灌注损伤 内皮功能障碍 氧化应激 

分 类 号：R541.4[医药卫生—心血管疾病]