六甲铵对哺乳动物神经肌肉接头的抗箭毒作用。

An anti-curare effect of hexamethonium at the mammalian neuromuscular junction.

Ferry C B, Marshall A R

Br J Pharmacol. 1973 Feb;47(2):353-62. doi: 10.1111/j.1476-5381.1973.tb08333.x.

Abstract

Experiments were performed on the isolated phrenic nerve and diaphragm preparation of the rat.2. In preparations partly blocked with (+)-tubocurarine, the twitch amplitude increased after hexamethonium. This enhancement was not seen in preparations partly blocked with Mg(++) or with gallamine. High concentrations of hexamethonium produced failure of contraction.3. Extracellular endplate potentials were recorded from blocked preparations. The administration of hexamethonium resulted in an increased amplitude of these potentials only in curarized muscle.4. Hexamethonium had no anticholinesterase activity nor did it depolarize muscle cells or increase the quantal release of transmitter.5. It is concluded that hexamethonium exerts a specific anti-curare action. Experiments on the recovery of the twitch after washing out antagonists indicate that this process is limited by diffusion. The difference in rates of diffusion of hexamethonium and (+)-tubocurarine does not account for their interaction. The basis of the anti-curare action of hexamethonium is discussed.

摘要

实验是在大鼠膈神经和膈肌分离标本上进行的。
在部分被（+）-筒箭毒碱阻断的标本中，六甲铵作用后抽搐幅度增加。在部分被Mg（++）或加拉明阻断的标本中未观察到这种增强作用。高浓度六甲铵会导致收缩功能丧失。
从阻断的标本记录细胞外终板电位。六甲铵给药仅在箭毒化的肌肉中导致这些电位幅度增加。
六甲铵没有抗胆碱酯酶活性，也不会使肌肉细胞去极化或增加递质的量子释放。
得出结论，六甲铵具有特异性抗箭毒作用。冲洗拮抗剂后对抽搐恢复的实验表明，该过程受扩散限制。六甲铵和（+）-筒箭毒碱扩散速率的差异不能解释它们的相互作用。讨论了六甲铵抗箭毒作用的基础。