Cembala Thor M, Forde Steven C O, Appadu Balraj L, Lambert David G
Department of Cardiovascular Sciences (Pharmacology and Therapeutics Group), Division of Anaesthesia, Critical Care and Pain Management, University of Leicester, Leicester Royal Infirmary, Leicester, LE1 5WW, UK.
Eur J Pharmacol. 2007 Aug 13;569(1-2):37-40. doi: 10.1016/j.ejphar.2007.04.048. Epub 2007 May 22.
Neuromuscular blocking drugs produce muscle weakness by interaction with nicotinic-acetylcholine receptors. Cardiovascular side effects have been reported. In this study the neuromuscular blocking drug vecuronium and the controls gallamine and pancuronium slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant human muscarinic M2 receptors K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01). These data indicate that vecuronium, gallamine and pancuronium interact with an allosteric site on the muscarinic M2 receptor (located on the heart) and this may explain some of their cardiac side effects.
神经肌肉阻断药物通过与烟碱型乙酰胆碱受体相互作用产生肌肉无力。已有心血管副作用的报道。在本研究中，神经肌肉阻断药物维库溴铵以及对照药物加拉明和泮库溴铵减缓了阿托品诱导的[³H]N - 甲基东莨菪碱从表达重组人毒蕈碱M2受体的中国仓鼠卵巢细胞上解离的速率（解离常数K(off)值，单位为分钟⁻¹；维库溴铵（125 nM），阿托品0.45 ± 0.07 +阻断剂0.04 ± 0.02；加拉明（21 nM），阿托品0.42 ± 0.05 +阻断剂0.15 ± 0.04；泮库溴铵（21 nM），阿托品0.36 ± 0.03 +阻断剂0.03 ± 0.01）。这些数据表明，维库溴铵、加拉明和泮库溴铵与毒蕈碱M2受体（位于心脏）上的变构位点相互作用，这可能解释了它们的一些心脏副作用。
