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目的探讨一氧化氮（ＮＯ）、一氧化氮合酶（ＮＯＳ）在癫痫发生中的作用及ＮＯＳ抑制剂的作用。方法采用海人酸致痫大鼠模型并应用ＮＯＳ抑制剂Ｌ－硝基精氨酸甲酯（Ｌ－ＮＡＭＥ），分别在致痫后３０分钟、６０分钟取海马组织，匀浆后测定ＮＯ及ＮＯＳ水平。结果致痫３０分钟后海马ＮＯ含量显著升高，至６０分钟恢复正常；ＮＯＳ活性水平增高＞５０％；Ｌ－ＮＡＭＥ明显抑制大鼠的痫性发作，应用ＮＯＳ抑制剂组大鼠海马ＮＯ、ＮＯＳ含量明显下降。结论癫痫发作后脑内ＮＯ、ＮＯＳ活性增强，ＮＯＳ抑制剂通过抑制酶活性使ＮＯ生成降低，并完全抑制痫性发作。ＮＯＳ活性受抑制＞４８％即可产生明显效果。提示ＮＯ可能有内源性致痫作用。
Objective To investigate the role of nitric oxide (NO) and nitric oxide synthase (NOS) in the development of epilepsy and the effect of NOS inhibitor. Methods The rat model of epilepsy induced by kainate and the application of L-NAME, an inhibitor of nitric oxide synthase, were used to detect hippocampus tissue at 30 and 60 minutes after epilepsy. NOS level. RESULTS: After 30 minutes of epilepsy, the content of NO in hippocampus was significantly increased and returned to normal after 60 minutes. The activity of NOS increased by 50%. L-NAME significantly inhibited the seizure in rats. NO, NOS The content decreased obviously. Conclusion The activity of NO and NOS in brain increased after epileptic seizures. NOS inhibitor decreased the production of NO by inhibiting enzyme activity and completely suppressed the seizure. Inhibition of NOS activity> 48% can produce significant results. Tip NO may have endogenous effects of epilepsy.