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目的 探讨NO在癫痫的病理生理过程中的作用及可能作用机制。方法 将大鼠随机分为对照组 ,实验性癫痫组 ,L 硝基精氨酸甲酯 (L NAME)抑制组 ,分别取双侧海马及颞叶皮层组织测定NO ,NOS及相应氨基酸的含量。结果 致痫后NOS活性上升 >50 %。NO含量明显上升 ,60分钟组NO含量明显下降。L Arg,Glu含量均显著上升。GABA则明显下降。不同剂量的L -NAME均抑制痫性发作及相应指标的变化。癫痫患者脑脊液中NO ,NOS含量均较对照组明显上升。结论 NO参与癫痫发生的机制 ,但对其维持作用并不重要。其致痫机制仅部分与兴奋性氨基酸有关。
Objective To explore the role of nitric oxide in the pathophysiology of epilepsy and its possible mechanism. Methods The rats were randomly divided into control group, experimental epilepsy group and L NAME inhibition group. The levels of NO, NOS and corresponding amino acids in bilateral hippocampus and temporal cortex were measured respectively. Results NOS activity increased after seizures> 50%. NO content increased significantly, 60 minutes NO content decreased significantly. L Arg, Glu content increased significantly. GABA decreased significantly. Different doses of L -NAME inhibit seizures and changes in the corresponding indicators. Cerebral spinal fluid in patients with epilepsy NO, NOS content were significantly increased compared with the control group. Conclusions NO participates in the mechanism of epilepsy, but it is not important for its maintenance effect. The mechanism of epileptiform induced excitatory amino acids only partially related.