Nishimura N
Nihon Seikeigeka Gakkai Zasshi. 1987 Jan;61(1):39-48.
Using hypophosphatemic rat maintained on a low phosphate diet as a model for human rickets and osteomalacia, the skeletal muscle was histochemically and electron microscopically examined, in comparison with specimens obtained from normal control animals. In muscles obtained from hypophosphatemic animals, the type 2 muscle fibers were increased in number, and the type 1 fibers were atrophic. Electron microscopic studies revealed some atypical structures of mitochondria with fusion of cristae in the muscle spindles of intrafusal muscle fibers. The presynapse, the secondary cleft, and the endplate plasm were significantly atrophic in the extrafusal neuromuscular junction. Mitochondrial vacuolization was observed in the presynapse. These results indicated the presence of immature muscle fibers, dysfunction of the energy metabolism of the mitochondria and neurogenic disorders in hypophosphatemic muscles.
以低磷饮食喂养的低磷血症大鼠作为人类佝偻病和骨软化症的模型，与正常对照动物的标本相比，对其骨骼肌进行了组织化学和电子显微镜检查。在低磷血症动物的肌肉中，2型肌纤维数量增加，1型纤维萎缩。电子显微镜研究显示，梭内肌纤维肌梭中线粒体有一些不典型结构，嵴融合。在梭外神经肌肉接头处，突触前膜、次级裂和终板质显著萎缩。在突触前膜观察到线粒体空泡化。这些结果表明低磷血症肌肉中存在未成熟肌纤维、线粒体能量代谢功能障碍和神经源性疾病。
