摘要
本文应用高专一性N—乙酰胆碱受体配体α—BTX研究了梭曼、沙林和VX等3种主要神经性毒剂对小鼠、大鼠膈肌和伸趾长肌N—乙酰胆碱受体(N—AChR)的作用。发现这3种强胆碱酯酶抑制剂对N—AChR的作用各不相同。沙林不直接作用于N—AChR,也不引起受体数的改变。VX直接结合N—AChR,使受体结合部位数减少。VX使受体减少一半的剂量为0.054 mg/kg体重小鼠。梭曼能使N-AChR数增多,1～1.5倍LD_(50)梭曼使小鼠膈肌的N—AChR数增加25％。中毒后30 min受体增加达到高峰,可持续96h。大鼠梭曼中毒后第4 d受体数仍比对照组高22％。梭曼主要使突触外N-AChR明显增多,导致胆碱能效应器官对ACh敏感性增高,出现类似切断神经的超敏现象。这一结果对于探讨梭曼中毒的受体机理和救治有重要意义。
The highly specific ligand of the N-acetylcholine receptor (N-AChR) was used to determine the effect of scman, sarin and VX on N-AChR of the diaphragm, and extensor digitorum longus muscle of the mouse and rat The effects of the three anticholinesterase agents on N-AChR were different Sarin didn't directly act on N-AChR and cause a change in the number of N-AChR VX decreased the binding site of the receptor through directly binding N-AChR The ID50 was 0.054 mg/kg mouse. Soman increased the binding sites, e.g. 1-1.5 LD50 soman increased the N-AChR of mouse diaphragm for 25% of the control. The increase in N-AChR was up to a highest peak 0.5 h after poisoning and continued for 96 h. The receptor number was still 22% higher than that of the control on the fourth day after soman poisoning in the rat Soman mainly increased the number of extrasynaptic N-AChR, leading to the enhancement of sensitivity of cholinergic effector to ACh. This simulates the sensibilization resulting from denervation. These findings are of significance in probing the receptor mechanisms and treatment of the soman poisoning.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1990年第5期440-444,共5页
Academic Journal of Second Military Medical University
关键词
乙酰胆碱受体
梭曼
沙林
VX
nicotinic acetylcholine receptor
VX
soman
satin
mice
rats
