Abstract
A study was performed to evaluate the hypothesis that heparin opposes uncontrolled PGI2 production by vessels due to thrombin generation. We treated animals with warfarin, an inhibitor of liver synthesis of prothrombin and other vit. K-dependent clotting factors. In fact, if thrombin is presumed to be the stimulus for PGI2 production, warfarin should suppress this effect. As warfarin treatment did not affect significantly PGI2-like activity, we conclude that a different hypothesis is necessary to explain the phenomenon. On the other hand, i.p. sodium heparin effectively induced a decrease in PGI2-LA synthesis, whereas s. c. calcium heparin did not significantly influence it.
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