FIBRINOGENOLYTIC AFIBRINOGENEMIA AFTER ENVENOMATION BY WESTERN DIAMONDBACK RATTLESNAKE (CROTALUS-ATROX)

  • 1 January 1984
    • journal article
    • research article
    • Vol. 63  (1) , 1-14
Abstract
The absence of fibrinogen and the presence of plasmic fragments X, Y, D and E were demonstrated in a patient bitten by a western diamondback rattlesnake, C. atrox. The factor VIII level and the platelet count were within normal limits. There were distinct changes of protease inhibitors in the patient''s plasma. .alpha.-1-Protease inhibitor was elevated. Antithrombin-III was only slightly decreased after the envenomation, but .alpha.2-antiplasmin and .alpha.2-macroglobulin were initially significantly lowered, returning to normal values in 38 and 3 days, respectively. Plasmin-.alpha.2-antiplasmin complex was present until day 10 after the envenomation. However, purified plasminogen was not activated in vitro by the venom. Cultured endothelial and smooth muscle cells from human blood vessels released an increased amount of plasminogen activator upon incubation with the venom. The release did not result from cell lysis. Platelets in normal human platelet-rich plasma were aggregated by 10 .mu.g/ml of the venom, without serotonin secretion. The aggregation kinetics and serotonin secretion induced by ADP (ADP) or arachidonate were not not significantly affected by the venom at 1-10 .mu.g/ml. The predominant mechanism of afibrinogenemia in the patient after C. atrox bite resulted from primary fibrinogenolysis and not from a consumptive coagulopathy. The lytic state seemed to be induced through an indirect activation of plasminogen by vascular plasminogen activator, which was probably released from endothelial cells and smooth muscle cells by the snake venom.