Nakamura K, Hatano Y, Mori K
Department of Anesthesiology, Kyoto University Hospital, Japan.
Acta Anaesthesiol Scand. 1988 Feb;32(2):125-30. doi: 10.1111/j.1399-6576.1988.tb02700.x.
The present study was undertaken to determine the site of action of trimethaphan in causing neuromuscular blockade using isolated rat and frog muscle. Trimethaphan and d-tubocurarine attenuated the twitch tension developed by nerve stimulation, trimethaphan being 1/100 to 1/200 as potent as d-tubocurarine. Neostigmine potentiated the inhibitory effect of trimethaphan but reversed the effect of d-tubocurarine. Trimethaphan shifted the dose response curve of frog rectus abdominis muscle for carbachol downwards, while d-tubocurarine shifted the curve parallel to the right. Treatment with d-tubocurarine or succinylcholine protected acetylcholine receptors from persistent blockade by alpha-bungarotoxin while, in contrast, trimethaphan failed to protect the receptors. The findings indicate that trimethaphan acts on the motor endplate but, unlike d-tubocurarine, does not interact with the recognition site of acetylcholine receptors; the action of trimethaphan appears to be associated with the blockade of endplate ionic channels.
本研究旨在利用离体大鼠和青蛙肌肉确定三甲噻方引起神经肌肉阻滞的作用部位。三甲噻方和d -筒箭毒碱减弱了神经刺激所产生的抽搐张力，三甲噻方的效力为d -筒箭毒碱的1/100至1/200。新斯的明增强了三甲噻方的抑制作用，但逆转了d -筒箭毒碱的作用。三甲噻方使青蛙腹直肌对卡巴胆碱的剂量反应曲线向下移动，而d -筒箭毒碱使曲线平行右移。用d -筒箭毒碱或琥珀酰胆碱处理可保护乙酰胆碱受体免受α -银环蛇毒素的持续阻滞，而相比之下，三甲噻方未能保护这些受体。这些发现表明，三甲噻方作用于运动终板，但与d -筒箭毒碱不同，它不与乙酰胆碱受体的识别位点相互作用；三甲噻方的作用似乎与终板离子通道的阻滞有关。
