Volodina A V, Gurko N S, Kiprenskiĭ Iu V, Pozdniakov O M
Patol Fiziol Eksp Ter. 1991(6):50-3.
The work is concerned with light-optic and ultrastructural analysis of the causes of incomplete structural and functional restoration of skeletal muscles after extensive trauma and replantation of the limb. It was found that posttraumatic myogenesis was limited due to change of some of the satellite cells from the myogenic type of development to differentiation with the formation of fibroblast-like cells. In distinction from the embryonal cells, the myoblasts form the surrounding basal membranes earlier which prevents their fusion and the formation of the myosymplast. The features of the macrophageal reaction, its permanency lead to accumulation of collagen in the interstitium. Progressing secondary neurogenic atrophy develops at the tissue level. The developing posttraumatic microangiopathies are the cause of secondary destructive changes in the muscles. The disorders of tissue nutrition and the progressing atrophic and destructive-degenerative processes gear the autoimmune mechanisms in the late periods which is conducive to stable chronicity of the pathological process in the muscle.
这项工作涉及对广泛创伤和肢体再植后骨骼肌结构和功能未能完全恢复的原因进行光学显微镜和超微结构分析。研究发现,创伤后肌生成受限是由于一些卫星细胞从肌源性发育类型转变为分化形成成纤维细胞样细胞。与胚胎细胞不同,成肌细胞更早形成周围的基底膜,这阻止了它们的融合以及肌质体的形成。巨噬细胞反应的特征及其持续性导致间质中胶原蛋白的积累。在组织水平上出现进行性继发性神经源性萎缩。创伤后微血管病的发展是肌肉继发性破坏改变的原因。组织营养紊乱以及进行性萎缩和破坏 - 退行性过程在后期启动自身免疫机制,这有利于肌肉病理过程的稳定慢性化。