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.
