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 value ( dose which inhibits 50% of platelet agglutination ) was 60 ± 8.7 μg/ml. In vivo, the i.v. administration of ATA to rats reduced the thrombus formation in an arteriovenous shunt with an ED₅₀ 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 ED₅₀ value being of 18.3 ± 2.0 mg/kg. In an experimenal model of disseminated intravascular coagulation, ATA protected mice from the lethal effect of thromboplastin-induced thromboembolism with a ED50 value of 1.1 ± 0.15 mg/kg, being in that respect 12 times less potent than standard heparin (ED50 = 90 ± 15 μg/kg). These observations therefore show that ATA is active 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.