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在固定的胫骨前肌中,神经肌肉突触前毒蕈碱 M 受体阻断对罗库溴铵诱导的神经肌肉阻滞的影响。

Effects of neuromuscular presynaptic muscarinic M receptor blockade on rocuronium-induced neuromuscular blockade in immobilized tibialis anterior muscles.

机构信息

Department of Anesthesiology and Pain Medicine, Gil Medical Center, College of Medicine, Gachon University, Incheon, Korea.

Department of Anesthesiology and Pain Medicine, Asan Medical Center, College of Medicine, Ulsan University, Seoul, Korea.

出版信息

Clin Exp Pharmacol Physiol. 2018 Dec;45(12):1309-1316. doi: 10.1111/1440-1681.13012. Epub 2018 Aug 30.

DOI:10.1111/1440-1681.13012
PMID:30005130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6282578/
Abstract

This in vivo study tested the hypothesis that the modulation of acetylcholine (ACh) release by the M muscarinic receptor (mAChR) in the neuromuscular junction of disused muscles may affect the tensions of the muscles during the neuromuscular monitoring of a rocuronium-induced neuromuscular block and compared the results with those obtained from normal muscles. A total of 20 C57BL/6 (wild-type) and 10 α7 knock out (α7KO) mice were used in this experiment. As a pre-experimental procedure, knee and ankle joints of right hind limbs were fixed by needle pinning at the 90° flexed position. After 2 weeks, the main experiment was performed. Both tendons of the tibialis anterior (TA) muscles were obtained, and the muscle tensions were recorded while the dose-responses of rocuronium were measured three times in the same mouse by the serial administration of pirenzepine (0, 0.001 and 0.01 μg/g). Weight losses were observed after 2 weeks of immobilization in both groups, and a decrease in the mass of TA muscles at the immobilized side was observed compared to those of the contralateral nonimmobilized side. Tension depression of the TA muscles at immobilized side of the α7KO group was faster than those of the wild-type group, but these differences decreased after the administration of pirenzepine. The tension depressions were similar regardless of the pirenzepine doses at the same side in the group. Tension depression may become more rapid in the α7 AChR-expressed disused muscles by the decreased release of ACh release upon neuronal firing by the blockade of facilitatory M mAChR.

摘要

本体内研究检验了这样一个假设,即在失用肌肉的神经肌肉接头中,M 型乙酰胆碱(ACh)受体(mAChR)对 ACh 释放的调节可能会影响罗库溴铵诱导的神经肌肉阻滞期间肌肉的张力,并将结果与正常肌肉的结果进行比较。该实验共使用了 20 只 C57BL/6(野生型)和 10 只α7 敲除(α7KO)小鼠。作为预实验程序,通过将右后肢的膝关节和踝关节用针固定在 90°弯曲位置来固定右后肢。2 周后,进行主要实验。取出胫骨前肌(TA)的两条肌腱,并在同一只小鼠中通过连续给予哌仑西平(0、0.001 和 0.01μg/g)三次测量罗库溴铵的剂量反应,同时记录肌肉张力。在两组中,经过 2 周的固定后均观察到体重减轻,并且与对侧未固定侧相比,固定侧的 TA 肌肉质量减少。α7KO 组固定侧 TA 肌肉的张力抑制比野生型组更快,但在给予哌仑西平后,这些差异减小。在同一组中,无论哌仑西平剂量如何,同侧的张力抑制均相似。通过阻断促进性 M 型 mAChR 来抑制神经元放电时 ACh 释放,α7 AChR 表达的失用肌肉中的张力抑制可能变得更快。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/2c15a83c65ca/CEP-45-1309-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/83286f785d5a/CEP-45-1309-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/35ca03a4cf77/CEP-45-1309-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/2c15a83c65ca/CEP-45-1309-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/83286f785d5a/CEP-45-1309-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/35ca03a4cf77/CEP-45-1309-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e9/6282578/2c15a83c65ca/CEP-45-1309-g003.jpg

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