Activation of intrinsic or extrinsic blood coagulation in experimental venous thrombosis and disseminated intravascular coagulation: Pathogenetic differences

Abstract

Clinical observations and the findings in certain experimental animal stuides indicate that disseminated intravascular coagulation (DIC) and venous thromboembolism are not usually associated suggesting that different pathogenetic mechanisms may be responsible for their production. This thesis was evaluated in rabbits into which various procoagulant mixtures were infused. Ellagic acid, homologous serum and a factor IXa concentrate each induced a shortening of the partial thromboplastin time (PTT) and venous stasis thrombi but not defibrination and little systemic fibrin monomer (FM) elaboration. An entirely different pattern of response consisting of prolongation of the PTT, FM elaboration and defribrination but no thrombosis was found after the infusion of three tissue factor preparations, Xa or thrombin. It is proposed that activation of the intrinsic pathway of blood coagulation results in a “hypercoagulable state” which results in the formation of venous thrombi but does not cause DIC. The latter is triggered by activation of the tissue or final common pathway and is associated with elaboration of an anticoagulant activity which prolongs the PTT and which may prevent the formation of venous thrombi.