756 Muscle Degeneration

Muscle degeneration and a shock syndrome, which frequently results in death, follow the release of limb tourniquets. Albumin and other plasma components are transferred into the affected muscle tissue (1-4) while toxic products of autolysis and hemolytic substances appear in the circulating blood (5-7). I t is possible that this abnormal transfer results in part from damage of capillaries and muscle fiber membranes. The application of cold delays autolysis and fluid exchange, modifies the shock symptoms, and reduces mortality (8). Chemical changes, such as the large decrease in phosphorus (9) and morphologic alterations, as revealed with the light microscope (9, 10), have been carefully studied. Wide interfibrillar spaces are observed in tissues taken immediately after release of the tourniquet, and some fibers show discoid decay of their fibrils. The primary alterations are followed several hours later by advancing granular and hyaline degeneration. The present communication extends the light microscopic observations of the succinic dehydrogenase distribution in normal fibers (11) to the degenerated fibers. With the electron microscope an at tempt is made to visualize the finer details in the development of discoid, hyaline, and granular degeneration seen after release of the tourniquet. The alterations thus produced are common to an extremely wide variety of muscle lesions. Further experience will determine whether degenerations of different etiology, such as those caused by bacterial toxins, vitamin E deficiency, or Coxsackie virus infection will expose specific details characteristic of each lesion.