论文部分内容阅读
目的 :探索有机磷酸酯类化合物急性中毒的 -氨基丁酸能系统机理 ,为有机磷酸酯类化合物急性中毒的治疗提供理论依据。方法 :采用大鼠脑神经末梢微囊GABA受体为模型 ,大鼠体内染毒 ,观察动物抽搐发作和不发作时GABA受体的变化。结果 :大鼠皮下注射梭曼 99μg·kg 1或二嗪农灌胃 1.0 95g·kg 1,发现3 H GABA的结合值在抽搐发作时显著降低 ;或大鼠腹腔注射丙氟磷 6mg·kg 1,3 H GABA的结合值显著降低。结论 :有机磷酸酯类化合物在一定浓度下能显著降低大鼠脑GABA受体的结合 ,GABA受体参与了某些有机磷酸酯类化合物的急性中毒过程。
Objective: To explore the mechanism of - aminobutyric acid system of acute poisoning of organophosphate compounds and to provide a theoretical basis for the treatment of acute poisoning of organophosphate compounds. Methods: The GABA receptor of rat brain nerve endings microcapsules was used as a model. The rats were exposed to the GABA receptor. The changes of GABA receptors were observed in seizure and non-seizure animals. RESULTS: Rats were subcutaneously injected with soman 99 μg · kg 1 or diazinon gavage 1.0 95 g · kg -1, and the binding value of 3 H GABA was found to be significantly reduced at the onset of seizure; or intraperitoneal injection of propafen 6 mg · kg -1 , The binding value of 3 H GABA was significantly reduced. CONCLUSION: Organophosphate compounds can significantly decrease the binding of GABA receptor in rat brain at a certain concentration. GABA receptor is involved in the acute poisoning of certain organophosphate compounds.