Published in:
Open Access
01-12-2004 | Review
The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?
Authors:
Raul Altman, Héctor L Luciardi, Juan Muntaner, Ramón N Herrera
Published in:
Thrombosis Journal
|
Issue 1/2004
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Excerpt
Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH
2. Subsequently, thromboxane synthase acts on PGH
2 to form TXA
2, a transient biological product that induces platelet aggregation and is a powerful vasoconstrictor. Aspirin acts primarily by interfering with the biosynthesis of cyclic prostanoids: TXA
2, prostacyclin, and other prostaglandins. It irreversibly inhibits COX-1 by acetylation of serine-530 and induces a long-lasting functional defect in the platelets. The resultant decrease in production of prostaglandins and TXA
2 probably accounts for much of aspirin's antithrombotic effect [
1,
2]. The plasma half-life of aspirin is only 20 min in circulating blood. It is rapidly deacetylated and converted to salicylate in vivo. Salicylate does not affect COX-1 or COX-2 activity [
3]. …