摘要
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
Objective:Study on acute toxicity mechanism of GABA and its receptor of UDMH in order to give the evidences of treating UDMH acute toxicity.Methods:Inject UDMH into rats by intracheal,then determine GABA and GAD in rats brain,observe the change of 3H-GABA binding to GABA receptor in rat's microsac.Results:The level of GABA and GAD activities decreased significantly (P<0.01),UDMH could decreased the binding of GABA receptor in vitro or in vivo before rat seizure;but when rat seizure,the binding of GABA receptor increased.Conclusion:The change of GABA and its receptor may play an important role in the mechanism of UDMH.
出处
《中国现代医学杂志》
CAS
CSCD
2001年第6期8-9,共2页
China Journal of Modern Medicine
基金
军乱后勤“九五”攻关课题资助项目
