Prolonged mechanical ventilation alters diaphragmatic structure and function.
Prolonged mechanical ventilation alters diaphragmatic structure and function.
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DOI：
10.1097/ccm.0b013e3181b6e760
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发表时间：
2009-10
影响因子：
8.8
通讯作者：
Levine S
中科院分区：
文献类型：
--
作者：
Powers SK;Kavazis AN;Levine S
综述目前关于长时间机械通气对膈功能和生物学影响的研究进展。系统文献综述。长时间机械通气可促进膈肌萎缩和收缩功能障碍。在实验动物和人类中，仅仅18小时的机械通气就会导致膈肌萎缩。延长机械通气时间也与膈肌收缩功能障碍有关。动物模型研究显示，机械通气引起的膈肌萎缩是由于膈蛋白分解增加和蛋白质合成减少。最近的研究已经确定calpain， caspase-3和泛素蛋白酶体系统是促进机械通气诱导的膈肌蛋白水解的关键蛋白酶。未来的科学挑战是描述机械通风诱导的激活这些蛋白酶和抑制横膈膜蛋白合成的信号通路。未来的研究将明确机械通气引起的膈肌无力的信号机制，为开发在长时间机械通气期间维持膈肌质量和功能的新药提供必要的知识。
To review current knowledge about the impact of prolonged mechanical ventilation on diaphragmatic function and biology. Systematic literature review. Prolonged mechanical ventilation can promote diaphragmatic atrophy and contractile dysfunction. As few as 18 hrs of mechanical ventilation results in diaphragmatic atrophy in both laboratory animals and humans. Prolonged mechanical ventilation is also associated with diaphragmatic contractile dysfunction. Studies using animal models revealed that mechanical ventilation-induced diaphragmatic atrophy is due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, and the ubiquitin-proteasome system as key proteases that contribute to mechanical ventilation-induced diaphragmatic proteolysis. The scientific challenge for the future is to delineate the mechanical ventilation-induced signaling pathways that activate these proteases and depress protein synthesis in the diaphragm. Future investigations that define the signaling mechanisms responsible for mechanical ventilation-induced diaphragmatic weakness will provide the knowledge required for the development of new medicines that can maintain diaphragmatic mass and function during prolonged mechanical ventilation.