Blood Fibrinolytic Activity during Arvin Therapy

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Abstract
Summary: When Arvin is administered to patients, there is a rapid fall in plasma plasminogen concentration and fibrin degradation products appear in the blood which can be detected both by their anticoagulant effect and by their reaction with anti‐fibrinogen serum. There is a minimal but inconstant increase in the concentration of plasminogen activator and circulating plasmin cannot be detected. These findings are similar to those recorded in the defibrination syndrome and are explained by the assumption that both plasminogen and activator are adsorbed onto intravascular fibrin micro‐clots. Local plasmin release would then cause lysis of fibrin with the appearance of fibrin degradation products.There is no apparent reason why this mechanism should assist in the lysis of coexisting preformed thrombi. The apparent rapid lysis of thrombi which has been observed in some patients treated with Arvin can be explained if such thrombi are not static, but represent a balance between fibrin deposition and fibrinolysis. Therapeutic defibrination, by preventing extension of the thrombus, would allow the normal fibrinolytic mechanism to produce dissolution of the thrombus.