论文部分内容阅读
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。
In this paper, we studied the effect of three major neurotoxic agents, such as soman, sarin and VX, on the N-acetylcholine receptor (N -AChR) role. The effect of these three kinds of strong cholinesterase inhibitors on N-AChR was found to be different. Sarin does not act directly on N-AChR, nor does it cause changes in the number of receptors. VX binds directly to N-AChR, reducing the number of receptor binding sites. VX reduced the number of recipients by 0.054 mg / kg body weight in half. Soman can increase the number of N-AChR, 1 to 1.5 times LD_ (50) Soman increases the number of N-AChR in mouse diaphragm by 25%. At 30 min after poisoning, the receptor peaked for 96 h. The number of rats on the 4th day after soman poisoning in rats was still 22% higher than that in the control group. Soman mainly makes the extranodal N-AChR significantly increased, resulting in cholinergic organs increased sensitivity to ACh, similar to cut off the nerve hypersensitivity phenomenon. This result is of great significance to explore the receptor mechanism and treatment of Soman’s poisoning.