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目的 :探索UDMH急性中毒的γ -氨基丁酸及其受体机制 ,为UDMH急性中毒的治疗提供论理依据。实验 :大鼠气管染毒 ,测定脑组织中GABA含量和GAD活性 ,观察脑神经末梢微囊受体的变化。结果 :UDMH使脑组织中GABA含量和GAD活力显著降低 (P <0 .0 1)。体外试验发现UDMH使GABA与其受体的结合下降 ;体内染毒试验发现在大鼠惊厥发作前GABA受体的结合显著下降 ,惊厥发作时GABA与受体的结合显著上升。结论 :UDMH通过影响GABA代谢过程和GABA受体功能部分导致中枢神经系统中毒症状出现
Objective: To explore the mechanism of γ - aminobutyric acid and its receptor in the acute poisoning of UDMH and provide the rationale for the treatment of acute poisoning of UDMH. Experiment: The trachea was exposed to the rats and the GABA content and GAD activity in the brain tissue were measured. The changes of the receptors of microcephalices in the cerebral nerve endings were observed. Results: UDMH significantly reduced GABA content and GAD activity in brain tissue (P <0.01). In vitro, it was found that UDMH decreased the binding of GABA to its receptor. In vivo exposure test showed that the binding of GABA receptor decreased significantly before seizure onset in rats and the binding of GABA to receptor increased significantly during seizure onset. CONCLUSIONS: UDMH causes central nervous system poisoning symptoms by affecting GABA metabolism and GABA receptor function