一氧化氮与索曼中毒

目的：探索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５．２ｍｉｎ（对照组）缩短到４．３ｍｉｎ（Ａｒｇ１６０ｎｍｏｌ），死亡率由５０％（对照组）增加至８１％（Ａｒｇ１６０ｎｍｏｌ）。ＮＡＭＥ预处理时，潜伏期从４．０ｍｉｎ延长到１４．５ｍｉｎ（ＮＡＭＥ２．２０μｍｏｌ），死亡率由８７％（对照组

Nitric oxide and soman poisoning.

AIM: To examine whether nitric-oxide (NO) is involved in the toxicity of soman. METHODS: With pretreatments of icv L-arginine (Arg, the substrate of nitric-oxide synthase NOS), NG-nitro-L-arginine methyl ester (NAME, the inhibitor of NOS), the latency of seizure, and the mortality of mice induced by soman poisoning were examined. The activities of brain NOS in soman-intoxicated mice were measured. RESULTS: In case of Arg pretreatments, the latency decreased (P < 0.05) from (5.2 +/- 1.8) min (control) to (4.3 +/- 0.8) min (Arg 160 nmol), and the mortality increased (P < 0.05) from 50% (control) to 81% (Arg 160 nmol). In case of NAME pretreatment, the latency increased (P < 0.01) from (4.0 +/- 1.1) min (control) to (14.5 +/- 5.0) min (NAME 2.20 mumol), and the mortality decreased (P < 0.05) from 87% (control) to 50% (NAME 2.20 mumol). The toxicity of soman in mice was enhanced by Arg and reduced by NAME all in a dose-dependent fashion. NAME antagonized the enhancement of soman poisoning by Arg. Intoxication of mice with soman increased the NOS activity in cerebrum, cerebellum, and hippocampus from 100% to 104% (P < 0.05), 115% (P < 0.01), and 111% (P < 0.01), respectively. CONCLUSION: The onset of seizure and death of mice induced by soman poisoning are related to the NO messenger system.