LPS引起心肌细胞肌浆网钙漏流的机制及在内毒素心功能损伤中的作用  

Mechanism of myocardial dysfunction in endotoxin injury by LPS

作　　者：姜昕 罗特丹 李鹏 JIANG Xin;LUO Te-dan;LI Peng(The Second Clinical Medical College of Jinan University, Shenzhen People＇s Hospital, Shenzhen 518020, China)

机构地区：[1]暨南大学第二临床医学院深圳市人民医院老年病科,广东深圳518020

出　　处：《中国地方病防治》2017年第12期1321-1323,共3页Chinese Journal of Control of Endemic Diseases

基　　金：国家自然科学基金资助项目(No.81401570);深圳市科技创新委资助项目(No.JCYJ 20130402101926972)

摘　　要：目的探究LPS引起心肌细胞肌浆网钙漏流的机制及在内毒素心功能损伤中的作用。方法应用膜片钳和激光共聚焦显微成像技术对LPS诱导的败血症休克大鼠心室肌细胞电生理活动以及钙信号的变化及其机制进行研究。结果(1)LPS引起心肌细胞收缩抑制;(2)LPS引起心肌细胞收缩偶联效率降低;(3)LPS引起钙火花发放增加。结论在LPS诱导的败血症休克大鼠模型上,心肌细胞RyR活动增加,钙火花发放增加,肌浆网钙漏流增强,肌浆网钙库容量部分耗竭,胞浆钙蓄积,心肌收缩抑制,导致心功能不全。Objective To explore the mechanism of LPS myocardial sarcoplasmic reticulum calcium leakage caused by endotoxin and its effect on heart function damage. Methods The patch clamp and confocal laser scanning microscopy were used to study the electrophysiological changes and calcium signaling of ventricular myocytes in septic shock rats induced by LPS. Results 1. LPS in- duced cardiomyocyte contraction inhibition; 2. LPS induced contraction coupling efficiency of cardiomyocytes decreased; 3. LPS caused calcium sparks increase. Conclusion In septic shock rats model induced by LPS, RyR activity of myocardial cell increased calcium sparks release and sarcoplasmic reticulum calcium leakage increased, and at the same time sarcoplasmic reticulum calcium pool volume part depletion, cytoplasmic calcium accumulation, inhibiting myocardial contraction and leading to cardiac dysfunction.

关 键 词：LPS 钙火花 钙漏流 RyRs 心功能损伤 

分 类 号：R542.2[医药卫生—心血管疾病]