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

脓毒症对神经肌肉传递的影响和非去极化神经肌肉阻滞剂的作用

基本信息

批准号：
15591647
负责人：
NARIMATSU Eichi
金额：
$ 2.18万
依托单位：
Sapporo Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2006
项目状态：
已结题

项目摘要

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

临床上已知败血症会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导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晚期脓毒症增加了终板电位振幅，增加了运动神经末梢的乙酰胆碱释放量，降低了终板膜的连接后乙酰胆碱敏感性，增加了神经肌肉电兴奋性。脓毒症对非去极化神经肌肉阻滞剂 Rocronium、泮库溴铵和 d-筒箭毒碱作用的影响，剂量依赖性地降低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条件下，泮库溴铵的右移最大，d-管箭毒碱的右移最小。对于每种神经肌肉阻滞剂，晚期脓毒症的右移均大于早期脓毒症。晚期脓毒症增强了罗库溴铵诱导的终板电位振幅的降低。晚期脓毒症不会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结后乙酰胆碱敏感性的降低。罗库溴铵没有改变晚期脓毒症引起的肌质膜电兴奋性的增加。这些结果表明了以下证据。脓毒症以各种方式影响神经肌肉传递中运动神经末梢、终板膜和肌浆膜的阶段以及非去极化神经肌肉阻滞剂在这些阶段的作用。脓毒症引起非去极化神经肌肉阻滞剂作用减弱的主要机制是肌浆膜电兴奋性的增加，但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。较少的