Coagulation changes and changes in pulmonary extravasation of albumin were measured in 132 rats: (1) with and without severe hindlimb tourniquet shock; and (2) with and without heparinization. The rats were divided into four groups: (1) nonheparinized controls; (2) nonheparinized rats with hindlimb tourniquet shock; (3) heparinized controls; and (4) heparinized rats with hindlimb tourniquet shock. In the nonheparinized rats with hindlimb shock, platelet count, Factor VIII, Factor I, prothrombin and proconvertin and plasminogen decreased, and pulmonary extravasation of albumin increased. In contrast, in the heparinized rats with hindlimb shock, only a decrease in platelets was evident. These findings suggest that severe tourniquet shock leads to intravascular coagulation with microembolization to the lungs. This would cause increased pulmonary capillary permeability or altered pulmonary microvascular forces, which account for the increased pulmonary extravasation of albumin. This extravasation is capable of producing the interstitial pulmonary edema, which is one of the changes which characterize the "shock lung syndrome.".
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