Modification of Venous Stasis Thrombosis by Platelet Active Drugs and by Heparin

In rats, stasis thrombosis of a renal vein was produced by the occlusion of a vascular segment after the induction of systemic hypercoagulability by intravenous injection of ellagic acid. The development of thrombosis depended upon the dose of ellagic acid, the duration of circulation before occlusion of the vascular segment and the duration of stasis. Morphologically the thrombus consisted mainly of red blood cells with occasional foci of platelet aggregates. Prostaglandin El, at doses which reduced platelet retention by glass beads (6 μg/min/300 g I.V.) only slightly reduced thrombus size. The platelet release inhibitor indomethacin (50 mg/kg I.V.) had no effect on thrombus size. Heparin (10 and 20 u/kg I.V.) produced a dose-related reduction of venous thrombosis. The platelet-active drug VK 774 at l0 to 50 mg/kg I.V. also reduced the thrombus size. Binding to ellagic acid or induction of coagulation changes are proposed as a possible mechanism of action. It is concluded that the participation of platelet function in the development of venous stasis thrombosis is small.

 

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