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[废用、衰老和恶病质中的神经肌肉异常]

[Neuromuscular abnormalities in disuse, ageing and cachexia].

作者信息

Kouyoumdjian J A

机构信息

Disciplina de Neurologia da Faculdade de Medicina, São José do Rio Preto.

出版信息

Arq Neuropsiquiatr. 1993 Sep;51(3):299-306. doi: 10.1590/s0004-282x1993000300001.

DOI:10.1590/s0004-282x1993000300001
PMID:8297230
Abstract

Cachexia, ageing and disuse and their effects on the human and animals neuromuscular system are reviewed. Disuse induces reduction of muscle fibers (mainly II) diameter with peripheral myofibrils lost; there is no core-targetoid or even reduction on myophosphorilase activity, both typical of denervation; the acetylcholine spontaneous release and trophic factors on myoneural junction are maintained; muscle fibers could change to angular shape. Ageing affects nerve and muscle by a continuous and progressive process of denervation and reinnervation; the number of motor units diminishes in sixties without any denervation electric activity; there is also reduction on the amount of ACh release on terminal neurons and mitochondrial oxidative capacity leading to compensatory type I muscle fiber number increase. Cachexia also induces reduction on muscle fibers diameter first on legs and then on arms and trunk; there is type II atrophy with occasional angular fibers, RNA/proteic synthesis reduction and normal DNA.

摘要

本文综述了恶病质、衰老和废用及其对人和动物神经肌肉系统的影响。废用会导致肌纤维(主要是II型)直径减小,外周肌原纤维丢失;不存在典型的去神经支配所具有的核心靶样结构,甚至肌磷酸化酶活性也无降低;神经肌肉接头处的乙酰胆碱自发释放和营养因子得以维持;肌纤维可能会变成角状。衰老通过持续且渐进的去神经支配和再支配过程影响神经和肌肉;在六十多岁时运动单位数量减少,但无任何去神经支配电活动;终末神经元上乙酰胆碱释放量以及线粒体氧化能力也会降低,从而导致I型肌纤维数量代偿性增加。恶病质也会首先导致腿部肌纤维直径减小,随后是手臂和躯干;出现II型萎缩,偶尔有角状纤维,RNA/蛋白质合成减少,而DNA正常。

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