Ashmore C R, Lee Y B, Summers P, Hitchcock L
Am J Physiol. 1984 May;246(5 Pt 1):C378-84. doi: 10.1152/ajpcell.1984.246.5.C378.
Skeletal muscle growth following denervation and denervation plus passive stretch was characterized in the patagialis muscle of normal and dystrophic chicks until 8 wk of age. In both genotypes, muscles denervated at 1 wk of age grew at reduced rates compared with contralateral control muscles whether or not they were passively stretched. Histograms of fiber size distributions as well as morphological criteria showed that passive stretch of denervated dystropic muscles substantially delayed the development of pathology. Denervation alone provided less protection. There was no evidence of fiber necrosis in any denervated dystrophic muscle, although many fibers did exhibit extreme hypertrophy and abnormal morphology. When denervated dystrophic muscles were allowed to reinnervate, growth and development of pathology was rapid. Because denervation, denervation with passive stretch, or passive stretch alone retards, but does not prevent, the development of pathology, it is concluded that dystrophy in the chick is a myogenic defect that is exacerbated by neurally mediated contractile activity.
在正常和营养不良雏鸡的翼膜肌中,对去神经支配以及去神经支配加被动拉伸后的骨骼肌生长情况进行了长达8周龄的表征研究。在两种基因型中,1周龄时去神经支配的肌肉,无论是否进行被动拉伸,与对侧对照肌肉相比,生长速率均降低。纤维大小分布直方图以及形态学标准表明,去神经支配的营养不良肌肉的被动拉伸显著延迟了病理发展。仅去神经支配提供的保护较少。在任何去神经支配的营养不良肌肉中均未发现纤维坏死的证据,尽管许多纤维确实表现出极度肥大和异常形态。当去神经支配的营养不良肌肉重新获得神经支配时,病理的生长和发展迅速。由于单独的去神经支配、去神经支配加被动拉伸或仅被动拉伸都会延缓但不能阻止病理发展,因此得出结论,雏鸡的营养不良是一种肌源性缺陷,神经介导的收缩活动会使其加剧。