Effects of sepsis on neuromuscular transmission and actions of nondepolarizing neuromuscular blocker

败血症在临床上可以减弱非去极化神经肌肉阻滞剂的作用。本研究旨在探讨脓毒症对神经肌肉传递的影响及非去极化神经肌肉阻滞剂的作用。结果脓毒症晚期使终板电位幅度增加，运动神经末梢释放量化乙酰胆碱增加，终板膜对乙酰胆碱的敏感性降低，肌浆膜电兴奋性增加。脓毒症对非去极化神经肌肉阻滞剂罗克宁、潘库溴铵和D-管乌拉林的作用呈剂量依赖性地降低神经刺激引起的收缩张力。早期和晚期脓毒症使这些曲线右移。在早期和晚期败血症条件下，潘库溴铵的右移最大，右旋卡林的右移最小。…在脓毒症晚期右移大于早期晚期脓毒症加重了罗库溴铵引起的终板电位幅度的降低。晚期脓毒症不改变罗库溴铵引起的量子乙酰胆碱释放的减少和罗库溴铵引起的连接后乙酰胆碱敏感性的降低。罗库溴铵不改变晚期脓毒症引起的肌浆膜电兴奋性增加。这些结果表明以下证据。脓毒症通过多种途径影响神经肌肉传递的运动神经末梢、终板膜和肌浆膜阶段，以及非去极化神经肌肉阻滞剂在这些阶段的作用。脓毒症导致非去极化神经肌肉阻滞剂作用减弱的主要和重要机制是肌浆膜电兴奋性增加，但不存在量化乙酰胆碱释放或连接后乙酰胆碱敏感性。脓毒症引起的非去极化神经肌肉阻滞剂的作用减弱取决于脓毒症的阶段和神经肌肉阻滞剂的种类。较少

Sepsis is known to attenuate the actions of nondepolarizing neuromuscular blockers clinically. This study was planned to investigate the effect of sepsis on neurommcular transmission and actions of nondepolarizing neuromuscular blockers.ResultsThe effect of sepsis on neuromuscular transmissionLate sepsis inc-eased endplate potential amplitude, increased quantal acetylcholine release from the motor nerve terminal, decreased postjunctional acetylcholine sensitivity of endplate membrane and increased electrical excitability of sarcoplasmic membrane.The effect of sepsis on actions of nondepolarizing neuromuscular blockersRocronium, pancuronium and d-tubocurarine dose-dependently decreased twitch tension elicited by nerve stimulation. Early and late sepsis shifted these curves rightwards. The rightward shift was largest in pancuronium and smallest in d-tubocurarine under the conditions of both early and late sepsis. The rightward shift in late sepsis was larger than that in early sepsis for … More each neuromuscular blocker.Late sepsis potentiated the rocuronium-induced decrease of endplate potential amplitude. Late sepsis did not alter the rocuronium-induced decrease of quantal acetylcholine release and the rocuronium-induced decrease of postjunctional acetylcholine sensitivity. Rocuronium did not alter the late sepsis-induced increase in electrical excitability of sarcoplasmic membrane.These results indicate the following evidences. Sepsis affects on the stages of motor nerve terminal, endplate membrane and sarcoplasmic membrane in neuromuscular transmission and on the actions of nondepolarizing neuromuscular blockers on these stages in various manners. The main and significant mechanism of sepsis inducing the attenuations of the actions of nondepolarizing neuromuscular blockers is the increase in electrical excitability of sarcoplasmic membrane, but does not exist in the quantal acetylcholine release or postjunctional acetylcholine sensitivity. The sepsis-induced attenuations in the actions of nondepolarizing neuromuscular blockers depend on the stage of sepsis and kinds of the neuromuscular blockers. Less