一氧化氮及一氧化氮合酶在遗传性癫痫易感大鼠惊厥发作中的作用

目的：探讨一氧化氮、一氧化氮合酶在遗传癫痫易感大鼠惊厥发作中的变化及作用。方法：选择惊厥评分在30－40的P77PMC大鼠35只，均分A－G7组，A组为对照组、G组预先30min腹腔注射一氧化氮合酶抑制剂L－NAME，分别于铃声刺激致惊后0．5、1、2、4,12h断头处死，取出脑组织分离双侧大脑皮层、海马等组织匀浆，测定一氧化氮及一氧化氮合酶，分别统计并进行t检验。结果：惊厥后0．5－1h皮层、海马一氧化氮、一氧化氮合酶逐渐升高，2h达峰值，4－12h恢复正常，应用L－NAME后，一氧化氮、一氧化氮合酶升高被抑制，但大鼠惊厥评分增高并致1例惊厥后死亡和明显延长惊厥持续时间。结论：惊厥后大鼠体内一氧化氮、一氧化氮合酶合成增加，给予合成酶抑制后能明显下降，但能加重惊厥程度和延长持续时间，提示一氧化氮于惊厥后升高，可能作为内源性抑制性性质，在惊厥发作自行终止机制中具有重要作用。

THE CHANGES AND ROLE OF NITRIC OXIDE NITRIC OXIDE SYNTHASE IN CONVULSION OF GENETICALLY EPILEPSY- PRONE RAT

Objective To investigate the changes and role of nitric oxide (NO)and nitric oxide synthase(NOS) in convulsions of genetically epilepsy-prone rat(P77PMC);Methods 35 rats with convulsion scores30-40 were randomly divided into 7 groups(A-G) respectively ,A -control ,G were pretreated with inhibitor of NOS ( N-nitro- arginine methyl ester, L-NAME) .The levels of NO and NOS in cerebral cortex ,hippocampus , were measured in 0.5,1,2,4,12hour respectively after convulsions;Results The concentrations of NO were gradually increased in 30-60 min, and reached the climax in 2 hours, but returned to the normal level in 4 hour, meanwhile, the activity of NOS was elevated about 76%,L-NAME can inhibit the enhancement of NO and NOS, and dramatically increased convulsion scores and extended duration of convulsions, and made one of them died in P77PMC. Conclusion Levels of NO and NOS were increased after convulsion, L-NAME made the decrease of NO by inhibitive enzyme activity, but aggravate convulsion intensity. It suggested that elevation of NO after convulsion, as a endogenous inhibitor, is involved in convulsion termination processes.