AURIN TRICARBOXYLIC-ACID INHIBITS EXPERIMENTAL VENOUS THROMBOSIS

In vitro, aurin tricarboxylic acid (ATA) inhibited ristocetin-induced human platelet agglutination in a dose-dependent manner. The IC50 valu e (dose which inhibits 50% of platelet agglutination) was 60 +/- 8.7 m u g/ml. In vivo, the i.v. administration of ATA to rats reduced the th rombus formation in an arteriovenous shunt with an ED(50) value of 9.0 +/- 1.6 mg/kg. In a venous thrombosis model, using a combination of a thrombogenic challenge and stasis, ATA displayed a significant, dose- dependent antithrombotic effect, the ED(50) value being of 18.3 +/- 2. 0 mg/kg. In an experimental model of disseminated intravascular coagul ation, ATA protected mice from the lethal effect of thromboplastin-ind uced thromboembolism with a ED(50) value of 1.1 +/- 0.15 mg/kg, being in that respect 12 times less potent than standard heparin (ED(50) = 9 0 +/- 15 mu g/kg). These observations therefore show that ATA is activ e in both arterial- or venous-type thrombosis models and suggest that von Willebrand Factor might be important not only in arterial but also in venous thrombosis.