WHILE CLINICAL investigators continue their empirical search for the optimum aspirin dose to prevent thrombogenesis, basic researchers have been looking at the effect of aspirin on two prostaglandins that are instrumental in clot formation.
Laboratory studies have determined that aspirin inhibits the production of cyclo-oxygenase, an enzyme that is essential for the production of thromboxane (TXA2), which promotes platelet aggregation, as well as for the synthesis of prostacyclin (PGI2), which inhibits platelet aggregation.
Fortunately, aspirin's effects on TXA2, which is produced by platelets, are longer lasting. Because platelets are not capable of producing new supplies of cyclo-oxygenase, the resumption of TXA2 production requires 48 hours— the time it takes to release a new generation of platelets.
In contrast, PGI2 is produced by endothelial cells, which are capable of cyclo-oxygenase production. As soon as aspirin therapy is discontinued, the endothelium resumes cyclo-oxygenase production. As a result,