Mechanism of Accelerated Lysis of Blood Clots from Heparinised Blood

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Abstract
Heparin in a concentration of 0.2–0.5 units per millilitre of blood, plasma, or serum produced two opposite effects on fibrinolysis: (1) Fibrinolysis of whole blood clots showed moderate inhibition asjudged by the levels of fibrin degradation products (FDP) of sera separated after blood clotting with and without heparin. Heparin-induced inhibition of fibrinolysis was also seen when comparing the lysis rates of heparin-free clots in heparinised plasma and serum with the lysis rate of these clots in the heparin-free control samples. (2) Blood coagulation in the presence of heparin produced clots which lysed faster in buffer and buffer containing plasminogen and urokinase than control clots formed in blood coagulation of heparin-free blood. Clot weight measurement as well as FDP estimation of clot supernatant sera eliminated a reduced fibrin content of heparin clots as a possible cause for the observed accelerated clot lysis. Clot solubility measurements in 1 % monochlor acetic acid also ruled out defective factor XIII cross-linkage as a possible cause for the accelerated lysis rates of heparin clots. The clot structure of heparinised blood reflected the effects of delayed coagulation on the cell distribution throughout the clot; this produced gravitational separation of red blood cells from an overlying layer of leucocyte aggregates and fibrin. On the basis of the finding that the heparin batch used by us inhibited lysis and of previous reports on the effects of platelets and leucocytes on clot lysis, we concluded that accelerated lysis of clots from heparinised blood was not due to a specific action of heparin, rather it was brought about by delayed coagulation which induced a cell distribution in the clot favouring accelerated lysis.