国家海洋战略不断推进，人类水下活动频次和深度不断加大，对潜水医学保障提出更高要求，其核心问题是减压病(DCS)防治。体内形成致病气泡是DCS根本原因，血管内气泡触发的广泛血管炎性损伤，在DCS的发生发展中起到了关键作用，但其机制尚不明确。我们研究发现，DCS大鼠模型中的血管炎性损伤，都伴随循环内皮微粒(EMPs)异常增加；将体外气泡灌流诱导的EMPs注入正常大鼠也可诱导相似血管炎性损伤，且与p38/MAPK信号通路密切相关。EMPs是血管内皮细胞活化或凋亡早期由胞膜出芽脱落于循环的小囊泡，很可能是DCS血管炎性损伤的核心调控环节。本课题拟利用大鼠离体血管段和原代肺动脉内皮细胞，建立体外气泡灌流模型模拟DCS气泡损伤，以验证EMPs在DCS血管炎性损伤中的生物效应，并揭示p38/MARK信号通路在EMPs形成机制中的作用，为阐明DCS发病机制提供新依据、也为探索DCS防治措施提供新思路。

With the progress of the national marine strategy , the frequency and depth of human activities underwater are increasing, which put forward the higher requirements of diving medical support technology, and the prevention and treatment of decompression sickness (DCS) has become the core of the problem in diving medical support. Conventional wisdom holds that the vascular occlusion induced by intravascular bubbles due to improper decompression is the root cause of DCS, with the further research, it was discovered that extensive vascular inflammatory damage triggered by intravascular bubbles has played a key role in the development of DCS, but its mechanism is not clear. Our previous study found that circulating endothelial microparticles (EMPs) were significantly increased in DCS rats with vascular inflammatory injury. Intravenous injection with EMPs from endothelial cell culture induced by bubble perfusion induced vascular inflammatory injury in normal rats, that closely related to the p38/MAPK signaling pathway. With a broad spectrum of biological activity, EMPs represent a population of vesicles released by budding of the plasma membrane during endothelial cell activation or early apoptosis, that is likely to be the core regulatory control of vascular inflammatory injury mechanism in DCS. Our research project is intended to use vascular segment and primary endothelial cell culture from rat pulmonary artery, and establish the vitro model of bubble perfusion to simulate the injury induced by DCS bubbles. With this model, we aim to verify the biological effects of EMPs in vascular inflammatory injury of DCS and reveal the role of p38/MARK signaling pathway in the formation mechanism of EMPs. So our research will provide a new basis for elucidating the pathogenesis of DCS and explore new ideas for the prevention and treatment of DCS.