脓毒症血管内皮功能障碍的研究进展  

Advances in the research of vascular endothelial dysfunction in sepsis

作　　者：郑兰 李廉钰 张鹏慧 张鼎新 秦窈窈 张玮玮[2] Zheng Lan;Li Lianyu;Zhang Penghui;Zhang Dingxin;Qin Yaoyao;Zhang Weiwei(College of Anesthesia,Shanxi Medical University,Taiyuan 030001,China;Department of Anesthesiology,Shanxi Provincial People's Hospital,Shanxi Medical University,Taiyuan 030012,China)

机构地区：[1]山西医科大学麻醉学院,太原030001 [2]山西医科大学附属山西省人民医院麻醉科,太原030012

出　　处：《国际麻醉学与复苏杂志》2024年第10期1111-1116,共6页International Journal of Anesthesiology and Resuscitation

摘　　要：脓毒症的发病率和病死率一直居高不下,是重症患者常见的死亡原因之一。脓毒症损伤血管内皮细胞(VEC)导致内皮功能障碍(ED),使各种舒张、收缩因子失调,机体出现持续性低血压,最终发展为脓毒症休克。内皮源性的舒张、收缩因子,如一氧化氮(NO)、前列腺素(PG)、内皮依赖性超极化因子(EDHF)、内皮素(ET)、血管紧张素、血栓素等均有不同程度的升高,最终以舒张因子作用为主,促进脓毒症休克发生。文章综述脓毒症致ED后VEC分泌的舒张和收缩血管因子致脓毒症休克的相关机制。Sepsis,with its consistently high morbidity and mortality rates,is a common cause of death in critically ill patients.Sepsis inflicts harm on vascular endothelial cells(VEC),resulting in endothelial dysfunction(ED).This dysfunction creates an imbal‑ance among numerous vasodilatory and vasoconstrictive factors,manifesting as ongoing hypotension in the organism and eventually ad‑vancing to septic shock.Endothelial‑derived vasoactive factors such as nitric oxide(NO),prostaglandins(PG),endothelium‑derived hy‑perpolarizing factor(EDHF),endothelin(ET),angiotensin,and thromboxane all exhibit varying degrees of increase,ultimately leading to a predominant role of vasodilatory factors that promote the occurrence of septic shock.This review summarizes the mechanism relat‑ed to septic shock caused by ED,focusing on the vasodilatory and vasoconstrictive factors secreted by VEC in the context of sepsis.

关 键 词：脓毒症 脓毒症休克 血管内皮细胞 内皮功能障碍 

分 类 号：R459.7[医药卫生—急诊医学]