Hashimoto Y, Shima T, Matsukawa S, Satou M
Tohoku J Exp Med. 1978 May;125(1):71-5. doi: 10.1620/tjem.125.71.
The effect of amikacin on the neuromuscular junction was studied in man during anesthesia and surgery. Amikacin alone did not show any neuromuscular blocking action in normal man in therapeutic doses (100-200 mg). However, during recovery from either d-tubocurarine block or phase II block with succinylcholine, the intravenous administration of 200 mg of amikacin caused a decrease in twitch tension. This neuromuscular block aggravated by amikacin was antagonized by edrophonium (10 mg) or calcium chloride (400 mg). Data obtained from the peroneal nerve-anterior tibial muscle preparation of rabbits suggested that the neuromuscular blocking potency of amikacin was one-twelfth of that of kanamycin in therapeutic doses. Although amikacin is thus less potent than kanamycin, caution should be taken in its use for patients with myasthenic state.
在麻醉和手术期间对人体研究了阿米卡星对神经肌肉接头的作用。在治疗剂量（100 - 200毫克）下，单独使用阿米卡星在正常人中未显示出任何神经肌肉阻滞作用。然而，在从筒箭毒碱阻滞或琥珀酰胆碱的II相阻滞恢复过程中，静脉注射200毫克阿米卡星会导致抽搐张力降低。这种由阿米卡星加重的神经肌肉阻滞可被依酚氯铵（10毫克）或氯化钙（400毫克）拮抗。从兔腓总神经 - 胫前肌标本获得的数据表明，在治疗剂量下，阿米卡星的神经肌肉阻滞效力是卡那霉素的十二分之一。因此，尽管阿米卡星的效力低于卡那霉素，但对于肌无力状态的患者使用时仍应谨慎。
