[Morpho- and pathogenesis of muscle injury in the crush syndrome].

Histologically, histochemically and electron-microscopically were studied the extremity muscles of patients and experimental animals with crush syndrome and period of compression lasting 1.5 h, 6 and 9 h, as well as on day 1-23 after decompression. The main type of muscular fiber injury was found to be discoid necrosis of ischemic genesis, that was characterized by the acute fiber relaxation, isotropic disc lysis, quick detritus resorption in the first 3 days with emptying of sarcolemmic tubes, delay of resorption in the following periods, low activity of inflammatory infiltrate cells, decrease of regenerative potential. Myofibrillar contracture leading to coagulation necrosis is more common in short compression (1.5 h) and after blood flow renewal, especially in distally located from the compression zone muscles. Three types of mitochondrial inclusions in myofibrils have been revealed, that reflect differences in pathogenesis of irreversible fibrillar injuries. Peculiar features of inflammatory reaction occurring in muscles are shown. They are: delay of inflammatory phase alternation, macrophagal insufficiency, absence of lymphocytes in the infiltrate. Depending on the type of myofibrillar injury, intracellular, intracellular-satellite and satellite-myoblast type of regenerative reactions were identified. The latter type is most characteristic of myofibrils that had undergone coagulation necrosis.