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

脓毒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黏膜传递的影响以及非去极化神经肌肉阻滞剂的作用。结果脓毒症对神经肌肉传导的影响脓毒症晚期使终板电位幅值升高，运动神经末梢乙酰胆碱释放量增加，终板膜结后乙酰胆碱敏感性降低，肌质膜电兴奋性升高。脓毒症对非去极化神经肌肉阻滞剂rocroonium、pancuronium和d-tubocurarine剂量依赖性降低神经刺激引起的抽搐张力的作用的影响。早期和晚期败血症使这些曲线向右移动。在早期和晚期脓毒症的情况下，右移最大的是泮库溴铵，最小的是d-管柯碱。每一种神经肌肉阻滞剂对晚期脓毒症的右移比早期脓毒症大。晚期脓毒症增强了罗库溴铵引起的终板电位振幅的下降。晚期脓毒症未改变罗库溴铵诱导的量乙酰胆碱释放减少和罗库溴铵诱导的结后乙酰胆碱敏感性降低。罗库溴铵不改变败血症晚期引起的肌质膜电兴奋性升高。这些结果表明了以下证据。脓毒症影响神经肌肉传递过程中运动神经末段、终板膜和肌质膜的各个阶段，并以各种方式影响非去极化神经肌肉阻滞剂在这些阶段的作用。脓毒症诱导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质膜电兴奋性的增加，而不存在于量乙酰胆碱释放或结后乙酰胆碱敏感性。非去极化神经肌肉阻滞剂在脓毒症诱导下的作用减弱取决于脓毒症的分期和神经肌肉阻滞剂的种类。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