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Human platelet factor 4 (PF4) is known to bind to heparin and inhibit its anticoagulant effect. This factor also inhibits the enzyme collagenase derived from cultured human skin and collagenase extracted from human granulocytes. The addition of heparin to the PF4-collagenase assay system has no effect on the observed inhibition of collagenase. Thus PF4 inhibits collagenase, in addition to neutralizing heparin.

1. Spontaneous local fibrinolysis occurred with, and was probably a consequence of thrombosis, with defibrination in vivo. 2. The efficacy of heparin in the prevention of defibrination was clearly demonstrated; warfarin therapy seemed to be ineffective. 3. The efficacy of heparin in the prevention of the associated fibrinolysis was clearly inferred. 4. Serum immunoelectrophoresis against anti-fibrinogen sera demonstrated abnormal precipitin bands, during defibrination and fibrinolysis, which disappeared during heparin administration. 5. The serum bands showed immunologic identity with in vitro plasmin digests of fibrinogen and the intensity and position of these precipitin bands appeared to depend on the amount of fibrinogen and the duration of the in vivo digestion period. 6. In this hypofibrinogenemic state, defibrination was indicated by markedly reduced levels of anti-hemophilic factor and Factor V and a fall in blood platelets. The presence of fibrinolysis was shown by the lowered levels of plasminogen, streptokinase and urokinase inhibitors, prolonged thrombin clotting times and fibrinolytic breakdown products in the serum even though little or no lysis occurred on fibrin plates and the euglobulin lysis times were within normal limits. 7. The administration of fibrinolytic inhibitors is strongly contraindicated under these circumstances.