Residual cyclooxygenase-1 activity and @entity1425 reduce the antiplatelet effect of @entity117 in XXXX with @entity583 .

@entity1 @entity2871 @entity46008 @entity1425 @entity117 @entity928 @entity1426 @entity460 @entity583 @entity857 @entity3075 @entity15094 @entity4357
@entity117 treatment is essential in @entity1 with @entity583 ( @entity583 ) to block platelet @entity2871 ( @entity928 )    synthesis. @entity1425 is known to enhance platelet reactivity induced by other agonists and to be elevated in @entity1 with @entity583 due to stress. Our objective was to study the influence of @entity1425 on platelet @entity928    synthesis in @entity1 treated with @entity117 for @entity583 at early onset (within 48 hours) and the potential biochemical mechanisms involved in the functional response. Washed platelets from 45 @entity1 with @entity583 and 10 @entity117 -free controls were stimulated with @entity1426 (AA) or AA + @entity1425 , and aggregation and @entity928    synthesis were evaluated. Full platelet aggregation was recorded in 8/45 @entity1 (18%) with a partial @entity928    inhibition (86%) vs. the @entity117 -free controls. Platelets from the remaining 37 @entity1 did not aggregate to AA and had @entity928    inhibition >95%. However, when platelets were simultaneously stimulated with AA + @entity1425 , in 25/37 @entity1 a large intensity of aggregation (73%) was observed and a 5.5-fold increase in @entity928    synthesis, although this remained residual (<5% of @entity117 -free controls). This residual- @entity928    was critical in the functional response, as demonstrated by the complete inhibition by @entity928    receptor blockade or additional @entity117 in vitro. The @entity4357 -3-kinase activity and the cytosolic @entity460 levels participated in this platelet response elicited by a receptor cooperation mechanism, while the Rho/ @entity46008 (ROCK) pathway or the blockade of the @entity857 receptors ( @entity15094 , @entity3075 ) were without effect. Residual-cyclooxygenase -1 activity and @entity1425 enhance @entity928   -dependent platelet function, which may reduce the clinical benefit of @entity117 in @entity1 with @entity583 .
