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目的 探讨有机磷酸酯类化合物急性中毒的γ 氨基丁酸能系统机理。方法 采用大鼠脑GA BA受体为模型 ,从体外、体内实验 (动物抽搐发作和不发作 ) ,观察GABA受体的变化。结果 在体外实验中 ,10mmol·L- 1的梭曼、丙氟磷或二嗪农均能显著降低大鼠GABA受体的结合 (P <0 0 1) ,1mmol·L- 1的梭曼或二嗪农仍能显著降低GABA受体的结合 (P <0 0 5)。大鼠皮下注射梭曼 99μg·kg- 1,或二嗪农灌胃 1 0 95g·kg- 1,发现3H GABA的结合值在抽搐发作时显著降低 ;大鼠腹腔注射丙氟磷 6mg·kg- 1,3H 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。
OBJECTIVE To investigate the mechanism of γ-aminobutyric acid (GABA) system in acute poisoning of organophosphates. Methods GA BA receptor in rat brain was used as model to observe the changes of GABA receptor in vitro and in vivo (animal convulsive seizure and non-seizure). Results In vitro experiments, somatostatin, propofol or diazinon with 10 mmol·L-1 all significantly reduced the binding of GABA receptor in rats (P <0.01), the soman of 1 mmol·L-1 Diazinon still significantly reduced GABA receptor binding (P <0 05). Rats were subcutaneously injected with soman 99μg · kg-1, or diazepam orally gavaged with 1 095g · kg-1, and the binding value of 3H GABA was found to be significantly decreased in seizure onset. Rats were intraperitoneally injected with 6 mg · kg- The binding value of 1,3H GABA was significantly reduced. Conclusions Organic phosphates can significantly decrease the binding of GABA receptor in rat brain at a certain concentration.