In the presence of strong P2Y12 receptor blockade, aspirin provides little additional inhibition of platelet aggregation.

ABSTRACT:

Background

Aspirin and antagonists of platelet ADP P2Y(12) receptors are often coprescribed for protection against thrombotic events. However, blockade of platelet P2Y(12) receptors can inhibit thromboxane A(2) (TXA(2))-dependent pathways of platelet activation independently of aspirin.

Objectives

To assess in vitro whether aspirin adds additional antiaggregatory effects to strong P2Y(12) receptor blockade.

Methods

With the use of platelet-rich plasma from healthy volunteers, determinations were made in 96-well plates of platelet aggregation, TXA(2) production and ADP/ATP release caused by ADP, arachidonic acid, collagen, epinephrine, TRAP-6 amide and U46619 (six concentrations of each) in the presence of prasugrel active metabolite (PAM; 0.1-10 μmol L(-1)), aspirin (

SUBMITTER: Armstrong PC 

PROVIDER: S-EPMC3064407 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature