Pathogenesis of Serum-induced Venous Thrombosis

The mechanisms involved in the initiation, propagation, and dissemination of intravascular clots remain obscure. The identification of each new clotting factor has raised the possibility that abnormalities in these factors might be found among patients with thromboembolism. Data have yet to be presented, however, demonstrating a causal relationship between intravascular thrombosis and an alteration in any of these clotting factors. Our efforts to uncover such a relationship proceeded from two observations. One was the impressive evidence that stasis plays an important role in the development of intravascular clotting. The other was the significant fact first established by Alexander, deVries, and Goldstein (1) and later confirmed by Owren (2) and Koller, Loeliger, and Duckert (3) that there is normally present in human serum a stable factor which accelerates prothrombin conversion. This factor has been variously called SPCA, Converting and factor VII. It has been repeatedly stated that blood stagnating in a vein included between two ligatures will remain liquid for weeks (4, 5). We have found, however, that although clot formation was never observed in such vein segments of dogs within 20 minutes of their isolation, fibrin clots