大鼠弥漫性脑损伤后脑组织内一氧化氮的变化及其意义

目的　初步探讨大鼠弥漫性脑损伤后一氧化氮 (NO)在继发性脑损害中的生理及病理作用。　方法　在使用Marmarou法创建大鼠弥漫性脑损伤模型基础上 ,于伤后不同时间取大鼠脑组织 ,采用Griess反应法观测NO在外伤后脑组织内表达的时程变化 ,并采用选择性诱导型一氧化氮合酶 (iNOS)的抑制剂氨基胍对其神经保护作用进行初步的探讨。　结果　大鼠弥漫性脑损伤后 ,NO水平即刻升高 (P <0 .0 1 ) ,于伤后 1 2h有所下降 ,但仍高于正常对照组 (P <0 .0 5 ) ,2 4 ,4 8h和 7d再次升高 ,与 1 2h相比 ,差异有显著性意义 (P <0 .0 5 )。外伤对照组神经轴索断裂数目明显高于正常对照组 (P <0 .0 1 ) ,也高于氨基胍实验组 (P <0 .0 5 )。　结论　 (1 )大鼠弥漫性脑损伤后脑组织内NO表达水平出现两个高峰 ,中晚期 (2 4 ,4 8h和 7d)NO出现二次升高。 (2 )NO可能参与了脑损伤后轴索损伤的继发过程 ;(3)氨基胍对外伤后神经轴索损伤有一定的保护作用。

Nitric oxide expression and significance in brain tissue after diffuse brain injury in rats

Objective To preliminarily explore the physiological and pathological role of nitric oxide (NO) in secondary brain injury after severe diffuse brain injury (DBI). Methods With the establishment of rat DBI model by means of Marmarou,the brain tissues were isolated from the rats at different time to observe NO expression in brain tissues by using Griess reaction and preliminarily discuss the role of NO in neuroprotection by using the selective inductive nitric oxide synthase (iNOS) inhibitor aminoguanidine. Results After DBI, NO in brain tissues increased immediately but decreased at the 12th hour,which was still higher than that in the control group (P<0.05). A secondary NO elevation appeared 24 and 48 hours and seven days after DBI, with significant difference compared with that at the 12th hour (P<0.05). The number of broken axons in the trauma control group was larger that that in the normal control group (P<0.01) and aminoguanidine experiment group (P<0.05). Conclusions NO expression in brain tissues shows two peaks after DBI. There appears a secondary NO increase at the middle and late stages (at the 24th and 48th hours and 7th day). NO may take part in the secondary axonal injury after DBI. Aminoguanidine exerts certain protective effect on axonal injury posterior to DBI.