作　　者： (苏坤）; (薛军）; (赵自刚）; (牛春雨）;

机构地区： 河北北方学院微循环研究所,河北张家口075000

出　　处： 《中国急救医学》 2017年第9期839-845,共7页

摘　　要： 血管紧张素转化酶（ACE）是肾素-血管紧张素系统（RAS）的重要成分，参与了多种疾病的病理过程。多种类型休克引起的过度、失控的炎症反应、血流动力学异常、肠屏障损伤、血管高通透性是引起多器官损伤，进而导致患者死亡的重要因素。在内毒素休克、失血性休克、缺血／再灌注损伤、烧伤性休克等多种严重病理过程中，ACE-血管紧张素Ⅱ（AngⅡ）及其受体（AT1R）在不同器官中的高表达，抑制ACE—AngⅡ-AT1R表达有利于减轻器官的损伤。本文针对ACE在休克后器官损伤中的作用进行综述，为ACE防治休克提供新的思路。 Angiotensin - converting enzyme （ACE） is an important component of renin - angiotensin system, and is associated with pathogenesis of multiple diseases. Various shocks induce excessive and uncontrolled inflammatory response, abnormal hemodynamics, intestine barrier injury and vascular hyper - permeability, which are important factors of multiple organ injury and death. The expressions of ACE, angiotensin Ⅱ （ AngⅡ ） , and Ang Ⅱ type 1 receptor （ AT1 R） are increased in different organs during the various severe pathological process of endotoxic shock, hemorrhagic shock, ischemia - reperfusion injury, and burn shock. Inhibition of ACE - Ang Ⅱ- AT1R expressions plays a positive role in alleviating organ injury. The present article reviews the role of ACE in shock - induced muhiple organ injury, therefore, provides a novel approach for treatment of shock through ACE.

关 键 词： 血管紧张素转化酶 休克 多器官损伤