Carmignani M, Scoppetta C, Ranelletti F O, Tonali P
Int J Clin Pharmacol Ther Toxicol. 1984 Mar;22(3):140-4.
At skeletal neuromuscular junction level in vivo and in vitro experiments have revealed an adverse reversible interaction between acetazolamide and anticholinesterase drugs. Acetazolamide (500 mg, i.v.) prevented the increase in amplitude induced by edrophonium (5 mg, i.v.) on the action potentials derived by surface electrodes from the opponens pollicis muscle of patients affected by myasthenia gravis, when the median nerve was stimulated at the wrist by low frequency repetitive pulses (5/s). Similarly, acetazolamide significantly reduced the contractile force potentiation induced by neostigmine on the rat phrenic-diaphragm preparation, indirectly stimulated by means of low frequency repetitive pulses on the motor nerve. Under such experimental conditions acetazolamide did not show any significant action of its own, but it counteracted the effects of anticholinesterase drugs only when tested before them. It is hypothesized that the effect of acetazolamide on the skeletal neuromuscular junction may occur at presynaptic and/or postsynaptic sites by a mechanism only partly ascribable to the well-known carbonic anhydrase inhibitory activity of this drug.
在体内和体外实验中，在骨骼肌神经肌肉接头水平发现乙酰唑胺与抗胆碱酯酶药物之间存在不良的可逆相互作用。当通过低频重复脉冲（5次/秒）刺激手腕处的正中神经时，乙酰唑胺（500毫克，静脉注射）可阻止依酚氯铵（5毫克，静脉注射）对重症肌无力患者拇对掌肌表面电极引出的动作电位幅度的增加。同样，乙酰唑胺显著降低了新斯的明对大鼠膈-膈肌标本的收缩力增强作用，该标本通过对运动神经进行低频重复脉冲间接刺激。在这种实验条件下，乙酰唑胺本身未显示出任何显著作用，但仅在抗胆碱酯酶药物之前进行测试时，它才会抵消其作用。据推测，乙酰唑胺对骨骼肌神经肌肉接头的作用可能发生在突触前和/或突触后部位，其机制仅部分归因于该药物众所周知的碳酸酐酶抑制活性。
