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REVIEW ARTICLE
Year : 2018  |  Volume : 131  |  Issue : 10  |  Page : 1225-1231

Molecular Mechanisms of Ventilator-Induced Lung Injury


1 Department of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China
2 Department of Critical Care Medicine, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China

Correspondence Address:
Dr. Shang-Long Yao
Department of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0366-6999.226840

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Objective: Mechanical ventilation (MV) has long been used as a life-sustaining approach for several decades. However, researchers realized that MV not only brings benefits to patients but also cause lung injury if used improperly, which is termed as ventilator-induced lung injury (VILI). This review aimed to discuss the pathogenesis of VILI and the underlying molecular mechanisms. Data Sources: This review was based on articles in the PubMed database up to December 2017 using the following keywords: “ventilator-induced lung injury”, “pathogenesis”, “mechanism”, and “biotrauma”. Study Selection: Original articles and reviews pertaining to mechanisms of VILI were included and reviewed. Results: The pathogenesis of VILI was defined gradually, from traditional pathological mechanisms (barotrauma, volutrauma, and atelectrauma) to biotrauma. High airway pressure and transpulmonary pressure or cyclic opening and collapse of alveoli were thought to be the mechanisms of barotraumas, volutrauma, and atelectrauma. In the past two decades, accumulating evidence have addressed the importance of biotrauma during VILI, the molecular mechanism underlying biotrauma included but not limited to proinflammatory cytokines release, reactive oxygen species production, complement activation as well as mechanotransduction. Conclusions: Barotrauma, volutrauma, atelectrauma, and biotrauma contribute to VILI, and the molecular mechanisms are being clarified gradually. More studies are warranted to figure out how to minimize lung injury induced by MV.

 

 Abstract in Chinese

机械通气肺损伤的分子机制

摘要

目的:机械通气作为生命支持的重要治疗方法,数十年来其已经在临床上被广泛应用。但是研究人员发现机械通气不仅是维持生命的方法之一,而且其在不恰当使用的情况下会引发肺组织损伤,即机械通气肺损伤。本综述拟探讨机械通气肺损伤的发生发展及有关分子机制。

数据来源:本综述所选取的文献均来自PubMed的数据库,截止时间为2017年12月。采用以下关键词进行搜索:呼吸机相关性肺损伤、发生发展、机制、生物伤。

研究选择:主要选择与呼吸机相关性肺损伤机制有关的论著以及综述,并对选取的文献加以分析总结。

结果:从传统的病理机制(气压伤、容积伤以及萎陷伤)到生物伤,研究人员对机械通气肺损伤发生发展的认识是逐渐加深的。较高的气道压、跨肺压以及肺泡的反复开放/闭合是导致气压伤、容积伤以及萎陷伤的主要原因。在过去的二十年中,越来越多的研究证实了生物伤在机械通气肺损伤中的重要作用,其潜在的分子机制包括但不限于以下几个方面:促炎性细胞因子的释放、活性氧簇的合成、补体激活以及机械转导。

结论:气压伤、容积伤、萎陷伤以及生物伤均可以引起机械通气肺损伤,相关的分子机制正逐渐被阐明。在此基础上,需要进一步研究如何减轻机械通气过程中的肺损伤。



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