非去极化肌松药致支气管痉挛的M胆碱受体介导机制

Mechanism of muscarinic receptors in bronchospasm caused by nondepolarizing muscle relaxants

非去极化肌松药(NDMR)引起支气管痉挛的机制仍未完全清楚,组胺释放并不能很好的解释之。最近研究揭示NDMR很可能通过M胆碱受体介导机制诱发支气管痉挛:在生理条件下,位于气道副交感神经节后纤维上的M2受体兴奋后,可抑制神经肌肉接头处乙酰胆碱的过量释放,抑制副交感神经兴奋(如插管时)引起的支气管收缩。NDMR选择性阻断此M2受体亚型,从而引起支气管痉挛的发生。对此机制的探讨为NDMR新药靶标研究和不良反应的防治提供了极为重要的药理学依据。

The mechanism of the nondepolarizing muscle relaxants (NDMR) caused bronchospasm is still unclear, since it can’t be explained perfectly by histamine release. Recent studies have revealed that NDMR may induce bronchospasm via muscarinic receptor-mediated mechanism. M_2 receptor located at postganglionic, parasympathetic nerve fiber in airway, can inhibit excessive acetylcholine release from neuromuscular junction, attenuate the bronchoconstriction caused by parasympathetic nerve stimulation (eg: intubation). NDMR can block this autoinhibitory M_2 receptor subtype and that results in the increasing risk of bronchospasm. The exploration on this complicated mechanism provides us an important pharmacological basis, which can guide us to search the new NDMR agents and control the adverse reactions.