Abstract

The degree of edema formed in the rat paw in response to subplantar injection of carrageenin has been shown to be inhibited by agents which affect the formation and resolution of fibrin. Prothrombin depletion (Pival), inhibition of prothrombin to thrombin conversion (heparin) and fibrinolysis (plasmin) all inhibit edema formation. The action of Pival is antagonized by vitamin K administration, and administration of thrombin leads to increased edema volumes. It is believed that in the carrageenin-induced rat-foot edema, edema formation and blood coagulation bear a close correlation, a conclusion reached previously by others for several laboratory animal models of inflammation.