Coagulation mechanism and effect of heparin in hemorrhagic shock.

Abstract

Hemorrhagic shock was produced in anesthetized and unanesthetized dogs by bleeding to fixed arterial pressure levels for specified periods using Wiggers' method. Blood was drawn through an ion exchange resin and at the end of the hypotension was reinfused simultaneously with the removed ions. Early in the hypotension there was usually some shortening of blood coagulation time. In the late hypotension and reinfusion period 75% of the dogs had a distinct prolongation of clotting time. Prothrombin activity and blood platelets showed a marked progressive decline during the shock period. Special tests indicated that the coagulation defect was mainly due to a decrease of labile factor in conjunction with a second deficiency, most likely prothrombin. There was no discernible deficiency of stable factor nor any release of heparinoids during the shock procedure. It is suggested that the hepatic anoxia and the resultant diminished production of labile factor and prothrombin contributes importantly to the clotting defect. Prior administration of heparin (10 mg/ kg) tended to lower mortality and increase survival time but did not afford critical protection against the development of irreversibility.