The site of action of trimethaphan-induced neuromuscular blockade in isolated rat and frog muscle.

Abstract:

: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.

authors

Nakamura K,Hatano Y,Mori K

doi

10.1111/j.1399-6576.1988.tb02700.x

subject

Has Abstract

pub_date

1988-02-01 00:00:00

pages

125-30

issue

2

eissn

0001-5172

issn

1399-6576

journal_volume

32

pub_type

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