Miller R D, Roderick L L
Br J Anaesth. 1978 Apr;50(4):317-24. doi: 10.1093/bja/50.4.317.
In 40 cases anesthetized with chloralose and urethane, pancuronium was infused i.v. at a constant rate to produce and maintain 90% depression twitch tension of the anterior tibialis muscle following supramaximal stimulation of the peroneal nerve. Neither respiratory alkalosis nor metabolic acidosis influenced the infusion rate required to produce 90% depression of twitch tension or antagonism of this depression yb neotigmine. Respiratory acidosis (pH 7.15; PaCO2 10 kPa) did not alter the required infusion rate but did prevent complete antagonism by neostigmine. Metabolic alkalosis (pH 7.65; PaCO2 4.8 kPa) reduced both the required infusion rate and prevented complete restoration of twitch tension by neostigmine. The duration of neostigmine antagonism was shortened by metabolic alkalosis. We conclude that respiratory acidosis and metabolic alkalosis prevent antagonism of pancuronium by neostigmine.
在40只使用水合氯醛和氨基甲酸乙酯麻醉的实验对象中，静脉恒速输注泮库溴铵，以在对腓总神经进行超强刺激后使胫前肌的颤搐张力产生并维持90%的抑制。呼吸性碱中毒和代谢性酸中毒均未影响产生90%颤搐张力抑制或新斯的明对该抑制的拮抗作用所需的输注速率。呼吸性酸中毒（pH 7.15；动脉血二氧化碳分压10 kPa）未改变所需的输注速率，但确实阻止了新斯的明的完全拮抗作用。代谢性碱中毒（pH 7.65；动脉血二氧化碳分压4.8 kPa）降低了所需的输注速率，并阻止了新斯的明使颤搐张力完全恢复。代谢性碱中毒缩短了新斯的明拮抗作用的持续时间。我们得出结论，呼吸性酸中毒和代谢性碱中毒会阻止新斯的明对泮库溴铵的拮抗作用。
