血管通透性增高是创伤休克致器官功能损伤的重要原因。微粒在多种疾病的发展中有重要作用，已成为多种疾病的诊断预后标记，微粒对凝血功能和炎症有明显调节作用，也有研究显示内皮微粒（EMP）对VEC功能有明显的调节作用。但EMP是否对创伤休克血管通透性有调节作用，目前未见相关研究。微粒作用于靶细胞的机制除了通过其膜表面的物质发挥作用外，还可通过携带microRNA发挥相关作用。前期研究发现创伤休克循环微粒明显增高，EMP可增加血管通透性，结合文献及前期预实验结果推测EMP在创伤休克血管通透性中有重要的作用，其机制可能通过EMP携带miR155作用于血管内皮细胞穿细胞途径（Cav-1）和细胞间途径（Occludin, Claudin-5）调节创伤休克血管通透性。为此，本项目拟通过整体动物、离体VEC，研究EMP在创伤休克血管通透性中的作用以及相关机制。通过研究为创伤休克血管通透性的防治提供新的思路。

The increase of vascular permeability played important role in organ function damage after traumatic shock. Microparticle participated in the occurrence of many diseases such as tumor and so on and it had been considered as marker of diagnosis and prognosis. Microparticle contributed to the disorders of couagulation and inflammation, and several studies also demonstrated that endothelial microparticle (EMP) interfered the function of vascular endothelial cell. It is not clear whether EMP take part in the occurrence of vascular permeability after traumatic shock. The mechanisms of MP regulating target cell function are major related with its membrane and also with carrying microRNA. We previous study demonstrated that expression of MP was increased significantly after traumatic shock, and exogenous EMP increased vascular permeability for normal animal. According to our previous results and reports, we hypothesis that “EMP play important role in the occurrence of vascular permeability after traumatic shock, its mechanism may be related that EMP regulate cav-1, occludin and claudin-5 via carrying miR 155”. We will provide new measure for the treatment of vascular permeability after traumatic shock.