Cardiology · 2008 · 41 citations · 0 references
MedicinePharmacologyClinical PharmacologyHemostasisPharmacodynamicsAntiplatelet TherapyAntithrombotic TherapyPlatelet ActivationPlatelet AggregationPlatelet FunctionPlatelet PhysiologyAntiplatelet DrugsArachidonic Acid SignalingFibrinogen BindingPlatelet Aggregation InhibitionPlatelet Function ModulationPlatelet Inhibition
Previous reports documented the inhibitory efficacy of different doses of aspirin on arachidonic acid (AA)-induced platelet aggregation, however, the sensitivity of platelets toward other agonists as well as the effects of aspirin on platelet and plasma plasminogen activator inhibitor-1 (PAI-1) release and levels were not investigated. Hence, the present study was undertaken to investigate the effect and duration of action of a single oral dose (650 mg) of aspirin on human platelet functions (n = 34, normal healthy male and female volunteers) including aggregation, fibrinogen binding and PAI-1 release, and on the plasma level of PAI-1. Aspirin demonstrated a rapid onset of action (at 2 h after ingestion) in specifically inhibiting ex vivo AA-mediated functions including (a) fibrinogen binding to gel-purified platelets, (b) platelet aggregation, and (c) platelet PAI-1 release. A peak reduction of plasma PAI-1 level at 2 h was demonstrated as well. The effect of aspirin on the ex vivo AA-mediated effects (a-c) was shown to last for up to 4 days. However, aspirin treatment resulted in a rebound effect in platelet function (a-c) to other platelet agonists such as adenosine diphosphate or the combination of agonists including adenosine diphosphate, epinephrine, and AA. In conclusion, a single oral dose of aspirin has long-acting effects on AA-induced platelet activation and reduces plasma levels of PAI-1 as well.(ABSTRACT TRUNCATED AT 250 WORDS)