新霉素对抗梭曼引起神经肌接头持续性去极化的机理分析

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梭曼等胆碱酯酶抑制剂中毒可致神经肌肉传递阻断导致肌麻痹,其中呼吸肌麻痹是梭曼等毒剂中毒的致死原因之一。最近,我们报道了神经肌接头的终板区持续性去极化(SD),是梭曼引起神经肌肉传递阻断的主要终板电位变化,并实验提出产生SD的机理主要是突触后乙酰胆碱受体(N—AChR)对蓄积的高浓度的乙酰胆碱(ACh)的反应,SD主要产生于突触后机制。而文献报道氨基糖甙类抗生素新霉素能够实验性地对抗梭曼引起的神经肌肉传递阻断,并且分析认为新霉素的对抗作用机理主要是通过拮抗突触前Ca(2+)的 Soman and other cholinesterase inhibitors can cause neuromuscular blockade leading to muscle paralysis, respiratory muscle paralysis is one of the causes of soman poisoning poisoning. Recently, we reported that the persistent depolarization (SD) of the terminal area of ​​the neuromuscular junction is the major endplate potential change that causes somatosensory neuromuscular blockade. Experiments have suggested that the mechanism of SD production is mainly the postsynaptic acetylcholine Reactivity of receptor (N-AChR) to accumulated high concentrations of acetylcholine (ACh), SD mainly arises in the postsynaptic mechanism. The reported aminoglycoside antibiotics neomycin can experimentally antagonize the block of neuromuscular transmission caused by soman, and that the mechanism of neomycin antagonism is mainly through antagonism of presynaptic Ca (2+)
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