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.
Keywords
Arterial injury - neointima - aurintricarboxylic acid - rabbit