大鼠颅脑外伤后早期脑微血管内皮细胞功能和结构的改变  

Changes of function and ultrastructure of cerebral microvascular endothelial cells early after traumatic brain injury in rats

作　　者：马辉[1] 钱志远[1] 黄胜明[1] 王爱东[1] 

机构地区：[1]苏州大学附属第二医院神经外科,215004

出　　处：《中华创伤杂志》2010年第7期635-639,共5页Chinese Journal of Trauma

摘　　要：目的 通过对大鼠脑损伤后早期脑血管内皮细胞的功能和结构的观察,探讨脑外伤早期微循环障碍形成的发生机制.方法 用改良Marmarous法建立大鼠闭合性脑损伤动物模型,伤后1 h、4 h、8 h、12 h、24 h、3 d及7 d分别自损伤组和假手术对照组取10只大鼠取脑,5只行免疫组化、5只行荧光定量PCR测定脑血管内皮细胞活化标志物假性血管性血友病因子（vWF）和血栓调节蛋白（TM）的表达变化.结果 大鼠脑损伤后TM和vWF在4 h开始表达,24 h达到峰值,7 d恢复正常.假手术对照组各时段TM和vWF的表达水平与损伤组比较,差异有统计学意义（P〈0.05）.结论 脑损伤早期脑微血管内皮细胞的活化是早期继发性脑损伤形成的重要机制.Objective To investigate the functional and ultrastructural changes of cerebral microvascular endothelial cells at early stage following traumatic brain injury （TBI） in rats. Methods The rat models with closed brain injury were established with the improved Marmarous method. The expressions of thrombomodulin （TM） and von Willebrand factor （vWF） were determined by immunohistochemical techniques （5 rats per group） and real-time quantitative RT-PCR （5 rats per group） respectively at 1, 4, 8, 12, 24 hours and at days 3 and 7 after injury. Results TM and vWF started expression at 4 hours, reached peak at 24 hours and recovered to normal at day 7 after TBI. The expression levels of TM and vWF at different time points in sham control group showed statistical difference compared with damage group （P 〈 0.05）. Conclusion The activation of the cerebral microvascular endothelial cells at early stage after TBI is the main mechanism of early secondary brain injury.

关 键 词：脑损伤 内皮细胞 血栓调节蛋白 假性血管性血友病因子 

分 类 号：R686[医药卫生—骨科学]