An Experimental study of the Pathogenesis of Venous Thrombosis Versus DIC: The Role of Intrinsic and Extrinsic Coagulation Pathways

Clinically, UIC is rarely accompanied by venous thromboembolism. These two entities were studied in rabbits in order to explain this paradox. Ellagic acid (0.1M, 10ml/kg), aged serum (1.3-10ml/kg), Factor IX_a concentrate (0.5-3. Oral/kg), Xa concentrate(1.0-5. Oml/kg) tissue (rabbit lung) extracts or simplastin. (l-4ml/kg) and purified thrombin(10-200u/kg) were infused. Venous segments were ligated is seconds after infusion, examined after 10 minutes stasis and thrombosis was graded (0-4+). Fibrinogen concentration, PTT, TT, PT and fibrin monomer (FM) were measured. Ellagic acid, serum and IXa each caused 4+ thrombi at low doses whereas even at the highest doses, they caused no change in fibrinogen concentration and only moderate FM (2+) elaboration. The PTT shortened after all these infusions. By contrast, X_a, thrombin and the tissue extracts caused fibrinogen consumption (approx. 25-50%). substantial FN (4+) elaboration but no venous thrombosis. The PTT, but not the TT or PT, was prolonged £1-1/2 baseline) for 2-3h. after the infusions. Mixing post-infusion and baseline plasmas (1:1), prolonged the PTT of the latter. These findings suggest that activation of the intrinsic pathway readily induces thrombosis in areas of stasis but not DIC, The latter is more readily induced via the extrinsic pathway and is associated with the elaboration of a potent, labile inhibitor of intrinsic coagulation which may be responsible for the absence of stasis thrombi.

 

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