Pathogenesis of early thrombus formation in experimental vein graft

When inferior vena cava of rabbit was replaced by 3 cm long woven Tetron (polyethylene terephthalates) graft under bolus injection of heparin (50 U/kg), the graft was completely occluded at 1.5 +/- 0.35 h after the bolus injection of heparin. In order to elucidate the pathogenesis of this early thrombus formation, the same venous grafting was performed in rabbits receiving anticoagulants and/or anti-platelet agents and the thrombus formation was analyzed by scanning electron microscopy as well as by measuring the weight of dehydrated thrombus. The grafts in rabbits receiving an additional bolus heparin were patent until the anticoagulant effect disappeared and the thrombus formed in these grafts was composed of platelet aggregates anchored to synthetic fibers and of erythrocytes trapped into fibrin network. The patency of the graft was maintained at least 5 hours in rabbits receiving intravenous injection of aspirin (20 mg/kg) or oral administration of ticlopidine (100 mg/kg/day x 5 days prior to the grafting). The weight of dehydrated thrombus of the graft in aspirin and ticlopidine treated rabbits was 25 +/- 5 and 12 +/- 4 mg respectively, which were significantly lower than that of control group (59 +/- 9 mg). Ultrastructural studies revealed in these grafts piles of erythrocytes with fibrin network which were layered over the synthetic fibers without bridges of platelet aggregates. Also, the treatment with anti-platelet agents, especially ticlopidine, resulted in inhibition of organization of fibrin network. These observations indicate that thrombus in venous graft is formed by anchorage of platelet aggregates to synthetic fibers followed by activation of coagulation to form network of polymerized fibrin entrapping erythrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)