Inhibition of platelet aggregation by ASA is due to a selective blockade of platelet cyclooxygenase (B). Selectivity of this action results from acetylation of this enzyme during the initial passage of the platelets through splanchnic blood vessels. Acetylation of the enzyme is irreversible. ASA present in the systemic circulation does not play a role in platelet inhibition. Since ASA undergoes extensive presystemic elimination, cyclo-oxygenases outside platelets, e.g., in en-dothelial cells, remain largely unaffected. With regular intake, selectivity is enhanced further because the anuclear platelets are unable to resynthesize new enzyme and the inhibitory effects of consecutive doses are added to each other. However, in the endothelial cells, de novo synthesis of the enzyme permits restoration of prostacyclin production.
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