摘要
目的：探索一氧化氮（ＮＯ）在氧惊厥中的作用。方法：利用一氧化氮合酶（ＮＯＳ）活性测试盒，采用分光光度比色法测定在几种不同气体及压力的暴露条件下，大鼠海马、纹状体和额叶皮质中ＮＯＳ活性的变化；并在６００ｋＰａ高压氧暴露下，观察脑室分别注射ＮＯＳ抑制剂Ｎω－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ）和超氧化物歧化酶（ＳＯＤ）对大鼠氧惊厥始发时间、惊厥严重程度和存活时间的影响。结果：大鼠濒临氧惊厥前及氧惊厥时所观察脑区的ＮＯＳ活性均显著升高；Ｌ－ＮＡＭＥ可显著延迟大鼠惊厥始发时间、延长存活时间并减轻惊厥严重程度；ＳＯＤ的作用与之相反。两者抗惊厥及促惊厥的效应存在量效关系。结论：ＮＯ参与氧惊厥发作的过程。
Objective: To evaluate the role of nitric oxide (NO) in the oxygen-induced convulsions. Methods: The nitric oxide synthase (NOS) activity in hippocampus, striatum and frontal cortex tissues of rats exposed to different gases or pressures was determined by means of spectrophotometry with NOS detecting case. Initial time of convulsions (ITC), severity of convulsions (SOC) and survival time (ST) of rats exposed to 600 kPa hyperbaric oxygen were also observed after intracerebroventricular injection of NωnitroLarginine methyl ester (LNAME) and superoxide dismutase (SOD). Results: The NOS activity in hippocampus, striatum and frontal cortex tissues of rats increased significantly before or at convulsions (P<0.01) in all of the brain areas observed. Intracerebroventricular injection of L-NAME could delay ITC (P<0.01),prolong ST (P<0.01) and decrease SOC (P<0.01),whereas intracerebroventricular injection of SOD could make the opposite effect. Both the anticonvulsant effect of L-NAME and the proconvulsant effect of SOD were dose-dependant. Conclusion: NO might play a role in oxygen-induced convulsions and be one of the endogenous agents which cause oxygen-induced convulsions.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1998年第4期337-339,共3页
Academic Journal of Second Military Medical University
关键词
一氧化氮合酶
一氧化氮
高压氧
氧中毒
nitric oxide synthase
nitric oxide
oxygen-induced convulsions
hyperbaric oxygen
