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目的：探查索曼中毒机制是否有ＮＯ参与．方法：预先侧脑室注射Ａｒｇ、ＮＡＭＥ，观察索曼中毒小鼠惊厥潜伏期、死亡率及脑中ＮＯＳ活性变化．结果：Ａｒｇ预处理时，潜伏期从５２ｍｉｎ（对照组）缩短到４３ｍｉｎ（Ａｒｇ１６０ｎｍｏｌ），死亡率由５０％（对照组）增加至８１％（Ａｒｇ１６０ｎｍｏｌ）．ＮＡＭＥ预处理时，潜伏期从４０ｍｉｎ延长到１４５ｍｉｎ（ＮＡＭＥ２２０μｍｏｌ），死亡率由８７％（对照组）减少至５０％（ＮＡＭＥ２２０μｍｏｌ）．索曼的小鼠毒性被Ａｒｇ增强、被ＮＡＭＥ减弱，均有剂量依赖性．索曼中毒可使小鼠大脑、小脑及海马的ＮＯＳ活性分别增加４％，１５％及１１％．结论：索曼中毒小鼠的惊厥及死亡与ＮＯ信使系统有关
Aims: To investigate whether there is NO involvement in the soman poisoning mechanism. Methods: Arg and NAME were pre-injected into the lateral ventricle to observe the seizure latency, mortality and brain NOS activity in the soman-poisoned mice. RESULTS: Arg pretreatment shortened the incubation period from 5.2 min (control group) to 4. 3 min (Arg 160 nmol) and increased the mortality rate from 50% (control group) to 81% (Arg 160 nmol). NAME pretreatment, the incubation period from 4 0min extended to 14 5min (NAME2 20μmol), the mortality rate decreased from 87% (control group) to 50% (NAME2 20μmol). Soman’s toxicity was enhanced by Arg and attenuated by NAME, both in a dose-dependent manner. Soman’s poisoning can increase the NOS activity of mouse brain, cerebellum and hippocampus by 4%, 15% and 11% respectively. CONCLUSIONS: Convulsions and death in soman-poisoned mice are related to the NO messenger system