脑挫伤后进展性出血性损害（PHI）是颅脑创伤后常见和严重的继发损害。我们前期证实，创伤后凝血功能障碍与PHI存在关联，但PHI的血管损害的机理尚不清楚。磺酰脲类受体1（SUR1）具有广泛的生物学功能，最新研究发现其可能与血管内皮细胞结构与功能关系密切。我们推测：脑血管内皮细胞在创伤作用下，启动一系列机械敏感的过程，即通过机械敏感瞬时电位受体（TRP）通道上调了SUR1的表达，造成血管内皮细胞凋亡及血管结构损害，最终发生进展性出血。为证实此假说，本项目运用rt-PCR、western-blot，基因干扰等技术，从细胞和器官水平观察SUR1在脑血管内皮细胞中的表达变化，及机械敏感TRP通道对SUR1的调控及由此引起的脑血管内皮细胞破坏的机制。本项目将进一步揭示PHI的发生机制，为脑挫伤后PHI的治疗提供新的策略。

The progressive hemorrhagic injury (PHI) of brain contusion is a severe and commonly-happened second injury in brain trauma. We have demonstrated in our earlier work that coagulation disorders after trauma is ralated to PHI. But the vascular injury mechanism in PHI is still unknown. Sulfonylurea receptor 1 (SUR1) has extensive biological functions. Lately researchers discovered that SUR1 may related to the structure and function of vascular endothelial cells closely. We hypothesize that cerebral vascular endothelial cells initiate a series of mechanosensitive processes following TBI. The processes up-regulate the expression of SUR1 via TRP channels and the up-regulation of SUR1 leads to disfunction of vasucular, and thus PHI comes up. To confirm our hypothesis, this programm utilizes rt-PCR、western-blot、and RNA interference etc technologies to observe the expression of SUR1 in vascular endothelial cells. And we will also observe how mechanosensitve TRP channels modulate the expression of SUR1 and the breakdown of vascular endothelial cells. Our program will further reveal the mechanism of PHI development, and provide a new strategy to treat PHI following cerebral contusion.