机械通气治疗是一把双刃剑，它在提供了一种有效呼吸支持治疗的同时，还可能导致或进一步加重肺部的损伤。对于ARDS患者，当"小潮气量保护性肺通气"策略受到限制时，通过抑制生物性损伤成为必要的治疗措施。在前期工作中，我们发现大潮气量机械通气可以激活肾素-血管紧张素系统(Renin - angiotensin system，RAS)并导致调控内皮细胞通透性最重要的信号分子之一RhoA蛋白的激活；故本课题拟探讨大潮气量机械通气激活RAS系统后是否通过活化细胞内RhoA/ROCK信号转导通路引起细胞骨架蛋白重构，进而导致肺微血管内皮细胞通透性增加的分子机制，为揭示机械通气相关性肺损伤的发病机制提供新的实验资料。

Mechanical ventilation is a double-edged sword, and providing an effective treatment of respiratory support, it may also lead to further lung injury.For patients with ARDS, when the "protective lung ventilation with low tidal volume strategy is limited, inhibition of the biological damage become necessary treatment measures.In previous work, we found that the tidal volume mechanical ventilation can activate the renin - angiotensin system and led to RhoA activation which is one of the most important signaling molecules in the regulation of endothelial cell permeability.Therefore, this study was to investigate whether the tidal volume ventilation can activate the RAS system through RhoA / ROCK signaling pathway which caused cytoskeletal protein reconstruction and lead to increased permeability of the molecular mechanisms of pulmonary microvascular endothelial cells. The completion of this project will provide new experimental data to reveal the pathogenesis of ventilator-associated lung injury.