机械通气与膈肌萎缩  

Mechanical ventilation and diaphragmatic atrophy

作　　者：马少林[1] 朱晓萍[1] 

机构地区：[1]同济大学附属东方医院ICU,上海200120

出　　处：《国际呼吸杂志》2012年第1期70-72,共3页International Journal of Respiration

基　　金：上海市浦东新区优秀学科带头人项目（PWRD2007-08）

摘　　要：机械通气已成为急性、慢性重症呼吸衰竭患者的必要治疗手段，但机械通气可导致呼吸机相关的膈肌功能障碍，并与通气患者撤机困难密切相关。对动物模型和机械通气患者的研究证实控制通气后膈肌失用性萎缩：膈肌肌块减小、肌纤维萎缩和肌球蛋白重链表达降低。膈肌萎缩出现快速且程度远较外周骨骼肌明显。肌萎缩源于蛋白分解加剧，和（或）蛋白合成减少。失用时膈肌细胞内数种参与收缩蛋白降解的蛋白酶水解途径被活化，钙调蛋白酶系统和泛素蛋白酶途径被认为是最主要的途径。本文就失用性肌萎缩蛋白分解的机制及信号转导途径综述如下。Mechanical ventilation （MV） is a life-saving form of supportive therapy for respiratory failure. However, diaphragmatic dysfunction is common in mechanically ventilated patients and is a likely cause of weaning failure. Reduced diaphragm muscle mass and （or） muscle fiber atrophy and decrease in expression of myosin heavy chain after CMV has been observed in most experimental and human studies. Atrophy develops more rapidly as early as 18 hours and to a significantly greater extent in the diaphragm than in peripheral skeletal muscles which are also inactive during CMV. The activation of several intracellular proteolytic pathways involved in degradation of the contractile apparatus. The calpains and the proteasome system are considered important for proteolysis during disuse atrophy. The specific objectives of this article are to provide an overview of muscle proteases, and the signaling pathways contributing to disuse muscle atrophy, and highlight gaps in our knowledge of MV-induced muscle atrophy.

关 键 词：机械通气 膈肌萎缩 泛素蛋白酶途径 CALPAINS 

分 类 号：R459.7[医药卫生—急诊医学]