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

脓毒症在临床上可减弱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递的影响：晚期脓毒症使终板电位振幅增加，运动神经末梢乙酰胆碱定量释放增加，脓毒症对终板膜乙酰胆碱敏感性的影响非去极化神经肌肉阻滞剂罗克溴铵、泮库溴铵和d-筒箭毒碱剂量依赖性地降低由神经刺激引起的抽搐张力。早期和晚期脓毒症使这些曲线向右移动。在早期和晚期脓毒症的条件下，泮库溴铵和d-筒箭毒碱的α位移最大。晚期脓毒症患者的血压变化大于早期脓毒症患者， ...更多信息 晚期脓毒症加重罗库溴铵引起的终板电位振幅的降低。晚期脓毒症并没有改变罗库溴铵诱导的量子乙酰胆碱释放的减少和罗库溴铵诱导的连接后乙酰胆碱敏感性的降低。罗库溴铵不能改变脓毒症晚期引起的肌质膜电兴奋性的增加。脓毒症对运动神经末梢、终板膜和肌质膜等神经肌肉传递阶段的影响以及非去极化神经肌肉阻滞剂对这些阶段的作用方式不同。脓毒症引起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，而不存在于乙酰胆碱的量子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作用的减弱取决于脓毒症的阶段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