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钾通道阻断增强膈和肢体肌肉等张收缩性能。

Improvement of diaphragm and limb muscle isotonic contractile performance by K+ channel blockade.

机构信息

Division of Pulmonary & Critical Care Medicine, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA.

出版信息

J Neuroeng Rehabil. 2010 Jan 11;7:1. doi: 10.1186/1743-0003-7-1.

DOI:10.1186/1743-0003-7-1
PMID:20064261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2821379/
Abstract

The K+ channel blocking aminopyridines greatly improve skeletal muscle isometric contractile performance during low to intermediate stimulation frequencies, making them potentially useful as inotropic agents for functional neuromuscular stimulation applications. Most restorative applications involve muscle shortening; however, previous studies on the effects of aminopyridines have involved muscle being held at constant length. Isotonic contractions differ substantially from isometric contractions at a cellular level with regards to factors such as cross-bridge formation and energetic requirements. The present study tested effects of 3,4-diaminopyridine (DAP) on isotonic contractile performance of diaphragm, extensor digitorum longus (EDL) and soleus muscles from rats. During contractions elicited during 20 Hz stimulation, DAP improved work over a range of loads for all three muscles. In contrast, peak power was augmented for the diaphragm and EDL but not the soleus. Maintenance of increased work and peak power was tested during repetitive fatigue-inducing stimulation using a single load of 40% and a stimulation frequency of 20 Hz. Work and peak power of both diaphragm and EDL were augmented by DAP for considerable periods of time, whereas that of soleus muscle was not affected significantly. These results demonstrate that DAP greatly improves both work and peak power of the diaphragm and EDL muscle during isotonic contractions, which combined with previous data on isometric contractions indicates that this agent is suitable for enhancing muscle performance during a range of contractile modalities.

摘要

钾通道阻断的氨基吡啶类药物在低至中等刺激频率下极大地改善了骨骼肌等长收缩的收缩性能,使它们有可能成为功能性神经肌肉刺激应用中的变力剂。大多数恢复性应用都涉及肌肉缩短;然而,以前关于氨基吡啶类药物影响的研究涉及肌肉保持在恒定长度。在细胞水平上,等张收缩与等长收缩有很大的不同,例如涉及横桥形成和能量需求的因素。本研究测试了 3,4-二氨基吡啶(DAP)对大鼠膈肌、趾长伸肌(EDL)和比目鱼肌等张收缩性能的影响。在 20 Hz 刺激引发的收缩过程中,DAP 在所有三种肌肉的一系列负荷下都提高了工作能力。相比之下,DAP 增强了膈肌和 EDL 的峰值功率,但没有增强比目鱼肌的峰值功率。在使用 40%的单一负荷和 20 Hz 的刺激频率进行重复疲劳诱导刺激时,测试了维持增加的工作和峰值功率的能力。在相当长的一段时间内,DAP 增强了膈肌和 EDL 的工作能力和峰值功率,而比目鱼肌的工作能力和峰值功率没有显著影响。这些结果表明,DAP 在等张收缩过程中极大地提高了膈肌和 EDL 肌肉的工作能力和峰值功率,这与以前的等长收缩数据相结合表明,这种药物适合在一系列收缩模式下增强肌肉性能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/e3057d050193/1743-0003-7-1-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/c319ae19c891/1743-0003-7-1-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/cbc5009636c0/1743-0003-7-1-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/00508bcfd5ff/1743-0003-7-1-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/872a9f31007f/1743-0003-7-1-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/7130007a7ccc/1743-0003-7-1-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/e3057d050193/1743-0003-7-1-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/c319ae19c891/1743-0003-7-1-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/cbc5009636c0/1743-0003-7-1-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/00508bcfd5ff/1743-0003-7-1-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/872a9f31007f/1743-0003-7-1-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/7130007a7ccc/1743-0003-7-1-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fa5/2821379/e3057d050193/1743-0003-7-1-6.jpg

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本文引用的文献

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2
Isotonic fatigue in laminin alpha2-deficient dy/dy dystrophic mouse diaphragm.层粘连蛋白α2缺陷型dy/dy营养不良小鼠膈肌的等张疲劳
Muscle Nerve. 2007 Nov;36(5):672-8. doi: 10.1002/mus.20860.
3
Isotonic contractile impairment due to genetic CLC-1 chloride channel deficiency in myotonic mouse diaphragm muscle.
钾通道阻断对在体偏心和等张抽动及疲劳收缩的影响。
Front Physiol. 2012 Sep 28;3:383. doi: 10.3389/fphys.2012.00383. eCollection 2012.
强直性肌营养不良小鼠膈肌中因遗传性CLC-1氯通道缺陷导致的等张收缩功能障碍。
Exp Physiol. 2007 Jul;92(4):717-29. doi: 10.1113/expphysiol.2007.038190. Epub 2007 May 4.
4
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5
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