背景 机械通气致肺损伤（ventilator induced lung injury， VILI）的机制研究众多，传统认为生物学损伤为主要机制，机械性损伤为触发因素。VILI的致死因素之一就是肺水肿的发生发展或以全身炎症反应综合征及多器官功能衰竭而终结。 目的 探讨肺水肿发生的机械损伤机制及其干预措施。 内容 现就生物学损伤及机械性损伤致VILI肺水肿的发生机制的最新研究作一综述，以期预防肺水肿的发生，为临床麻醉及重症监护过程中VILI致肺水肿的发生奠定理论基础。 趋向 机械性损伤触发肺水肿的发生，做为机械通气诱发肺损伤的特殊感受器，研究综述了机械力直接损伤、瞬时感受电位（transient receptor potential， TRP）超家族介导机械刺激诱发神经源性炎症反应（neurogenic inflammation， NI）在肺水肿的发生中所起的闸门作用，阻断早期肺损伤的诱发因素对于围术期肺保护具有重要意义。
Background Mechanisms of lung injury induced by mechanical ventilation are multiple. Biological damage is a key cause in ventilator induced lung injury（VILI）. One of the lethal factor in the development of lung injury induced by mechanical ventilation is the vulnerant pulmonary edema， and usually ends on systemic inflammatory response syndrome and multiple organ failure. Objective To explore the mechanism of pulmonary edema and its interventions. Content This article reviews the latest research on the mechanism of VILI caused by biological damage and mechanical damage in order to prevent the occurrence of pulmonary edema， and establish theoretical basis for pulmonary edema induced by VILI during clinical anesthesia and intensive care units stay. Trend As a special receptors of lung injury induced by mechanical ventilation， mechanical damage trigger the occurrence of pulmonary edema. The study reviewed the mechanisim of transient receptor potential（TRP） superfamily in early lung edema， which take an important role in the perioperative lung preservation.
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