Influence of Fibrinogen Degradation Products (FDP) on Platelet Aggregation, Adhesiveness and Viscous Metamorphosis

Abstract

SummaryInfluence of SKPL on platelet function tests has been studied.1. Human platelets suspended in borate buffer lose after SKPL treatment the ability to aggregate under the influence of thrombin, ADP and connective tissue extract.2. Washed platelets incubated with SKPL did not influence the thrombin time of prothrombin free plasma.3. The digestion of platelet rich plasma with SKPL diminished the ability of platelets to aggregate under the influence of thrombin, ADP and connective tissue extract and the adhesiveness to glass.4. Viscous metamorphosis after addition of thrombin or ADP was delayed and less advanced in SKPL treated platelet rich plasma as compared with control undigested plasma.5. The addition of FDP preparation to platelet suspension or to platelet rich plasma impaired their ability to aggregate under the influence of thrombin, ADP and connective tissue extract.6. Adhesiveness of platelets to glass in the whole blood containing FDP was decreased in comparison with controls.7. FDP inhibits also the adhesion of platelets from platelet rich plasma to connective tissue fibers (collagen).8. Viscous metamorphosis induced by thrombin, ADP or connective tissue extract in platelet rich plasma could be delayed or inhibited by addition of FDP.9. Inhibiting effect of FDP on platelet functions were dependent on concentration of FDP and aggregating agent. FDP influence platelet functions in such concentration which inhibit significantly the thrombin time. Increase of the concentration of the inducing agent can overcome the inhibitory effects of FDP.10. The significance of the described findings for the hemostatic function of platelets is discussed.

Treatment of Thrombosis by Sequential Therapy with Ancrod Followed by Streptokinase Clinical Pharmacology and Rheology

“…Previous authors have experimented with defibrination with Defibrase followed by streptokinase and simultaneous Defibrase and streptokinase administration and have pro duced similar changes to those described by us [11,13]. There was no rise in FDP levels which are associated with a haemorrhagic tendency by inter ference with fibrin polymerisation and platelet function [10,12], This was due partly to the relative depletion of plasminogen which is consumed during digestion of the fibrin microclots and also partly due to the low levels of plasminogen activator which may then reach the thrombus via the microcirculation, the flow in which has been improved by reduction in viscosity by the prior administration of ancrod.…”

Role of Platelet Fibrinogen in the Reactions of Platelets to Thrombin*

“…It seems unlikely that this observation would explain the inhibition of thrombin-induced aggregation by plasmin, since plasmin-treated platelets do react to thrombin by release of serotonin and ATP. The products of plasmin-digested fibrinogen have been shown to interfere with polymerization of plasma fibrinogen after thrombin action (29,30) and with aggregation of platelets by thrombin (31), and it is conceiv-able that products of plasmin digestion adherent to the surface of the platelet might interfere with polymerization of platelet fibrinogen. Furthermore, plasmin itself digests fibrinogen into fragments that are not polymerized by thrombin (32).…”

Plasmin-Induced Platelet Aggregation and Platelet Release Reaction. EFFECTS ON HEMOSTASIS

“…It is generally accepted that the bleeding in patients receiving SK may depend on several causes, such as digestion of fibrinogen, digestion of fibrin in the hemostatic plug (13), and the formation of fibrinogen degradation products that may inhibit clotting (21,(31)(32)(33) and platelet aggregation (25,(33)(34)(35)(36)(37). However, recent observations indicate that the "antiaggregating activity" of degradation products is low and not specific (3,38).…”