实验性大鼠脑损伤后介质白三烯C_4的变化在继发性脑损害中的作用

目的探讨实验性大鼠脑损伤后,炎性介质白三烯C4(LTC4)的变化及在继发性脑损伤中的作用。方法应用流体冲击装置致大鼠脑损伤模型,应用放射免疫分析法检测大脑皮层LTC4的含量变化,采用氢清除法定量监测皮层血流量的相应改变,并用木条行走作业试验行大鼠神经功能观察,并用5-脂加氧酶抑制剂菲尼酮阻止LTC4产生。结果流体冲击致大鼠脑损伤后,冲击侧皮层LTC4含量在伤后30min、1h显著增加,同时皮层血流量均显著下降,伤后5d内大鼠完成木条行走作业的能力明显受损。给予菲尼酮预处理后,皮层中LTC4明显减少,并伴有局部血流量增加,且大鼠完成木条行走作业恢复正常的时间缩短。结论流体冲击致大鼠脑损伤后冲击侧皮层中LTC4的产生明显增加,不仅加重了皮层血循环障碍,同时也直接或间接参与了继发性脑损伤过程。

The Changes of lukotriene C4 and its action in secondary cerebral injury after cerebral injury of experimental rats

Objective To investigate the process of leukotriene C4 in secondary brain injury following experimental traumatic brain injury in rats.Methods Using experimental rat brain model injured by fluid percussion device, the content of LTC4 in cerebral cortical tissue wasassayed by radioimmunoassay,cortical blood flow was determined with hydrogen clear method and the beam walking task was employed to observe neurological functional changes.Results Following fluid percussion brain injury,the content of LTC4 in the cortical tissue was markedly increased at 30 minutes and 1 hour,at 4 hours decreased to the pre injury level,then the cortical blood flow decreased all the way.Within 5 days the ability to process in beam walking task was significantly lessened.After pre treatment with phenidone,the production of LTC4 in local cortex was reduced,meanwhile the cortical blood flow was,however,increased obviously.The periods of neurological dysfunction were shortened.Conclusion Following fluid percussion brain injury,the production of LTC4 in the percussion cortex is markedly increased,which is not only aggravated cortical circulation insult,but also directly and indirectly participated in secondary brain injury.