脓毒症心肌线粒体损伤的机制  

Mechanism of myocardial mitochondrial injury in sepsis

作　　者：王思 张盼 解俊敏[1] WANG Si;ZHANG Pan;XIE Junmin(Department of Cardiology,Affiliated Hospital of Hebei University,Baoding,Hebei 071000,China)

机构地区：[1]河北大学附属医院心血管内科,河北保定071000

出　　处：《中国临床研究》2024年第12期1936-1939,共4页Chinese Journal of Clinical Research

基　　金：河北省医学适用技术跟踪项目(GZ2022070)。

摘　　要：脓毒症和感染性休克仍是危重症患者死亡的主要原因,尽管到目前为止已经采用各种治疗策略,但效果欠佳。脓毒症诱导的心肌功能障碍(SIMD)是严重脓毒症的一种常见并发症,也是危重症患者死亡的主要原因之一。因此深入了解SIMD对脓毒症的治疗至关重要。线粒体作为心肌细胞能量代谢的主要场所,其结构异常和功能障碍在其中起到重要作用。线粒体功能障碍主要包括:氧化应激、线粒体解偶联、线粒体的质量控制系统紊乱、Ca 2+超载和线粒体膜通透性改变。Sepsis and infectious shock remain the leading causes of death in critically ill patients.Despite the adoption of various treatment strategies to date,the outcomeshave been suboptimal.Sepsis-induced myocardial dysfunction(SIMD)is a common complication of severe sepsis.It is one of the leading causes of death.Therefore,further understanding of SIMD is very important for the treatment of sepsis.Mitochondria,as the main sites of energy metabolism of cardiomyocytes,play an important role in structural abnormalities and dysfunction.Mitochondrial dysfunction mainly includes oxidative stress,mitochondrial uncoupling,disturbance of mitochondrial quality control system,Ca 2+overload and altered mitochondrial membrane permeability.

关 键 词：脓毒症 线粒体 心肌功能障碍 氧化应激 钙超载 线粒体质量控制 

分 类 号：R459.7[医药卫生—急诊医学]