实验性大鼠脑损伤后血脑屏障、脑水肿的变化

目的　探讨实验性大鼠脑损伤后脑水肿发生的特点 ,以及干预脑水肿发生的意义。方法　应用流体冲击装置致大鼠脑损伤 ,通过对大鼠脑组织中伊文氏蓝 (EvansBlue ,EB)含量、脑组织内百分水含量、神经功能改变等的观测 ,探讨菲尼酮对大鼠创伤性脑损伤的影响。结果　大鼠脑损伤后 4小时 ,直接冲击侧以及对侧脑EB含量达高峰 ,冲击侧脑组织百分水含量在伤后 4小时明显增加 ,伤后 4天内出现明显的神经功能障碍 ;菲尼酮不同程度地降低了脑组织EB含量、百分水含量 ,神经功能得到一定程度的恢复。结论　流体冲击致大鼠脑损伤后 ,引起明显的血管内伊文氏蓝外渗、脑水肿 ,大鼠神经功能损伤 ,菲尼酮可明显阻止以上变化 ,由此说明白三烯是引起大鼠血脑屏障 (blood brainbarrier,BBB)开放的原因之一 ,说明脑损伤后减轻脑水肿是必要的。

Changes of blood-brain barrier and cerebral edema following experimental brain injury in rats

Objective To investigate the characteristics of traumatic cerebral edema and the significance of interfering with brain edema following experimental brain injury.?Methods Using experimental rat brain model injured by fluid percussion device, contents of Evans blue and brain water in cerebral tissue were assayed,in the meantime the rat neurological behavior was observed.?Results Following brain injury, the content of Evans blue in direct and indirect percussion sides peaked at 4 hours, the percentage of brain water content was significantly increased at the same time. Among 4 days post injury the neurological function was obviously insulted. After pre treatment with phenidone, the contents of Evans blue and percent water in brain tissue were decreased in varying degrees,and the neurological function was partly improved.?Conclusion Following fluid percussion brain injury,Evans blue exuded from cerebral vessels and brain edema was produced, then the neurological function was injured. Phenidone, however, may prevent these insults from traumatic brain injury. These suggest that leukotrienes is one of the cause of blood brain barrier disruption and it is necessary for traumatic brain injury to decrease edema following brain injury.