Although the clot-promoting activity of foreign surfaces has been the subject of many studies during almost a century (1) its nature is not yet understood. While glass has been thought to activate platelets (2), recent studies have mostly been concerned with the effect of glass on plasma clotting factors.Quick maintained that contact with glass activates the precursor of prothrombin, prothrombinogen (3) as well as the precursor of plasma thromboplastin, possibly antihemophilic factor A (4). Conley and his associates (5-8) have reported that contact with glass markedly shortens the clotting time of silicone prepared "platelet free" plasma and increases its prothrombin utilization. They concluded that glass activates "plasma thromboplastin," a constituent residing in the globulin fraction. Biggs, Douglas, and Macfarlane (9) stated that the increased clotting activity developed in plasma by contact with glass is probably due to a change in Christmas Factor (PTC, antihemophilic factor B). Alexander, de Vries, and Goldstein (10) observed that contact with glass during clotting of blood favors the evolution of SPCA (convertin, Factor VII). Rapaport, Aas, and Owren (11) showed that exposure to glass markedly increases the activity of proconvertin as well as of PTC. Other communications (12, 13) attributed the clot-promoting activity of glass to removal of lipid or protein inhibitors of the first phase of coagulation, i.e., the evolution of thromboplastic activity.In the present study it is shown that a plasma clotting factor other than those mentioned above may be activated by contact with glass.
MATERIALS AND METHODSCollection of blood. Human venous blood was collected by the two-syringe method using silicone coated needles and glassware.