Thromb Haemost 2002; 88(04): 668-672
DOI: 10.1055/s-0037-1613273
Review Article
Schattauer GmbH

Aurintricarboxylic Acid Attenuates Intimal Thickening after Balloon Injury of the Rabbit Aorta

Alvaro Waissbluth
1   Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
,
Giorgio Ghigliotti*
1   Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
,
Dana R. Abendschein
1   Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
,
Paul R. Eisenberg
1   Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
,
David Schwartz**
1   Department of Internal Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA
› Author Affiliations
Further Information

Publication History

Received 07 January 2002

Accepted after revision 28 May 2002

Publication Date:
09 December 2017 (online)

Summary

Injury to the arterial wall initiates a cascade of events including platelet deposition and an increase in procoagulant activity of the vessel wall that is associated with intimal thickening and vascular wall remodeling. This study was designed to characterize the effects of aurintricarboxylic acid (ATA), an inhibitor of von Willebrand factor function, on vascular procoagulant activity and the development of intimal thickening after balloon-induced injury to the rabbit aorta.

Treatment with ATA, aspirin, or the combination of agents at doses that attenuated platelet aggregation decreased platelet deposition and procoagulant activity bound to the vessel wall after injury. Treatment with ATA reduced the intimal thickening observed 2 weeks after injury. Surprisingly, aspirin treatment had no effect on intimal thickening. These data indicate that inhibition of platelet deposition, while it is able to attenuate local thrombin elaboration, is not alone sufficient to attenuate subsequent intimal thickening that occurs in response to arterial injury.

* Present Address: Department of Cardiology, University of Genoa,. Genoa, Italy


** Present Address: Lilly Research Laboratories, Indianapolis, IN, USA


 
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