“…These effects include the dose-dependent inhibition of platelet function, 74 -78 the enhancement of fibrinolysis, 79 -81 and the suppression of plasma coagulation. [82][83][84][85] In contrast to the saturable and well-characterized (nanomolar aspirin concentration, rapid time course, physiologic conditions, and single serine modification) inhibition of COX-1 by aspirin, 86,87 the putative mechanisms underpinning the non-PG effects of aspirin on hemostasis are dose-dependent and less clearly defined. For example, the inhibition of shear-induced platelet aggregation depends on the level of aspirin provided, and enhanced fibrinolysis due to N-acetylation of lysyl residues of fibrinogen is seen in vivo with high doses of aspirin (650 mg twice daily) 79 and proceeds more rapidly in vitro under nonphysiologic alkaline conditions.…”