Becker L D, Miller R D
Anesthesiology. 1976 Jul;45(1):84-7. doi: 10.1097/00000542-197607000-00015.
Neuromuscular blockades induced by clindamycin alone and with d-tubocurarine or pancuronium were examined in the in-vitro guinea pig lumbrical muscle-nerve preparation. Clindamycin, 80-240 mug/ml, initially increased twitch tension. With higher concentrations (180-240 mug/ml) twitch tension subsequently decreased. With 15 to 20 per cent depression of twitch tension by clindamycin, neostigmine (5-20 ng/ml) or calcium (81 mug/ml) slightly but not completely antagonized the blockade. Clindamycin, 40 mug/ml, a dose that did not depress twitch tension, potentiated d-tubocurarine- or pancuronium-induced neuromuscular bloackade. Plasma concentrations of clindamycin of 10-40 mug/ml were recommended for treating serious infections. The authors conclude that the administration of clindamycin may augment nondepolarizing blockade in man, and antagonism by neostigmine and calcium may be incomplete.
在体外豚鼠蚓状肌-神经标本中研究了单独使用克林霉素以及与右旋筒箭毒碱或泮库溴铵合用所致的神经肌肉阻滞作用。80-240微克/毫升的克林霉素最初可增加抽搐张力。浓度更高时(180-240微克/毫升),抽搐张力随后降低。当克林霉素使抽搐张力降低15%至20%时,新斯的明(5-20纳克/毫升)或钙(81微克/毫升)可轻微但不能完全拮抗这种阻滞作用。40微克/毫升的克林霉素这一剂量不会降低抽搐张力,但可增强右旋筒箭毒碱或泮库溴铵所致的神经肌肉阻滞。推荐10-40微克/毫升的血浆克林霉素浓度用于治疗严重感染。作者得出结论,克林霉素的给药可能会增强人体的非去极化阻滞作用,新斯的明和钙的拮抗作用可能不完全。