Figure 2.
Assessing the relationship between inhibition of COX-2 activity and prostacyclin biosynthesis in man. Systemic inhibition of COX-2 activity was determined as inhibition of LPS-induced PGE2 production in whole blood ex vivo, and inhibition of prostacyclin production was determined as reduced urinary excretion
of of 2,3-dinor-6-keto-PGF1α, a major enzymatic metabolite of prostacyclin. In response to the administration of five different COX inhibitors, the relationship
between inhibition of COX-2 activity and inhibition of prostacyclin biosynthesis was linear, with substantial inhibition of
the latter occurring at levels of incomplete suppression of the former. [Reproduced from (24) with permission from the American College of Cardiology.]