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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). It 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 attempt 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. MethodsAs in antecedent electrophoretic studies of blood and tissue extracts after shock-producing injuries (2-4), the technique of Rosenthal (12) was used for traumatizafion of hind legs of C57

TWELVE FIGURE8SSince the time when Purkinje (1845) first noted a peculiar type of muscle fiber in sheep hearts, a considerable body of information has accumulated on the structure and distribution of the fibers which now bear Purkinje's name. Nevertheless, the literature still contains numerous contradictions regarding the distribution of the Purkinje fibers and their significance in cardiac conduction.According to most accounts, the S-A node is composed of fusiform, branching fibers which have fewer myofibrils and a smaller breadth than ordinary atrial fibers. The node is considered to be a localized structure composed of a characteristic fiber type. Davies ('42), among others, has substantiated this view. On the other hand, specific structural characteristics for the fibers of the nodal region have been denied by some investigators, particularly Todd ( ' 3 2 ) , Glomset and Glomset ('40a) and Glomset and Birge ('45). Most investigators agree that fibers of the nodal region connect with ordinary atrial fibers but there is disagreement as to whether they also join a system of Purkinje fibers extending over the atria. Likewise, there is disagreement as to whether an impulse originating in the S-A nodal region reaches the A-V node by spreading in a wave-like manner over atrial muscle in general (Lewis, '25; Davies, '42; and