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Prostacyclin (PGI2) is rapidly hydrolysed in aqueous solution at neutral pH. Previously we have reported that PGI2 is stabilized by plasma components; yet PGI2 is rapidly metabolized in vivo. These findings prompted us to study the fate of PGI2 upon incubation in whole blood. The data on the distribution of PGI2 between blood cells and plasma indicate that PGI2 not only binds to platelets but also to erythrocytes. The Kinetics of binding were studied in more detail by incubating [3H] PGI2 at 37°C with washed erythrocytes resuspended in autologous plasma. Binding of [3H] PGI2 plateaued within 2 min. and was concentration dependant. The binding of [3H] PGI2 was not influenced by PGE1 or 6 keto PGF1α. [3H] 6 keto PGF1α showed no substantial binding to erythrocytes when compared with [3H] PGI2. Upon repeated incubation of [3H] PGI2 with erythrocytes less binding occured than would have Been expected from time and concentration dependancy. The latter finding is explained by the demonstration of breakdown of [3H] PGI2 - most likely into [3H] 6 keto-PGF1α - and by measurements of the biological activity of PGI2 Although metabol isation of PGI2 complicates the evaluation of binding kinetics it coufd be shown, by using inhibition of platelet serotonin release, that erythrocytes and platelets compete for PGI2. Binding of PGI2 to erythrocytes and subsequent metabolisation explains the apparent lability of PGI2 in whole blood. It is to expected that under physiological conditions erythrocytes suppress the effectiveness of PGI2 to act as a circulating platelet inhibitor.

Binding And Metabolisation Of PGI2 By Erythrocytes