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目的：从神经递质方面研究偏二甲基肼（ＵＤＭＨ）经非暴露式气管染毒急性中毒的生化机理。方法：Ｗｉｓｔａｒ大鼠分为正常对照组和低、中、高３个剂量组（染毒剂量分别为８０、１６０、２４０ｍｇ／ｋｇ），分３个染毒时相点即３０、６０、和９０ｍｉｎ，测定大鼠脑中γ－氨基丁酸（ＧＡＢＡ）、谷氨酸（Ｇｌｕ）含量和谷氨酸脱羧酶（ＧＡＤ）、γ－氨基丁酸转氨酶（ＧＡＢＡ－Ｔ）活性。结果：（１）各剂量组ＧＡＢＡ含量和ＧＡＤ活性明显低于对照组（Ｐ＜０．０１），且存在一定的量效和时效关系。（２）高剂量组ＧＡＢＡ－Ｔ活性低于对照组（Ｐ＜０．０５）。（３）中、高剂量组Ｇｌｕ含量明显高于对照组（Ｐ＜０．０１）。结论：ＵＤＭＨ引起中枢神经系统中毒症状主要是由于ＧＡＤ活性降低引起ＧＡＢＡ含量降低所致。可能还与Ｇｌｕ含量升高有关。
OBJECTIVE: To study the biochemical mechanism of acute poisoning induced by non-exposed tracheal exposure to dimethylhydrazine (UDMH) from neurotransmitters. Methods: Wistar rats were divided into normal control group and low, medium and high dose groups (dose of 80, 160 and 240 mg / kg respectively), divided into 3 exposure time points of 30, 60, and 90 min The contents of GABA, Glu, GAD and GABA-T in rat brain were measured. Results: (1) GABA content and GAD activity of each dose group were significantly lower than those of the control group (P <0.01), and there was some dose-effect and time-effect relationship. (2) GABA-T activity in high-dose group was lower than that in control group (P <0.05). (3) The content of Glu in medium and high dose groups was significantly higher than that in control group (P <0.01). Conclusion: The symptoms of central nervous system poisoning caused by UDMH are mainly caused by the decrease of GABA content caused by the decrease of GAD activity. May also be associated with increased Glu content.