Abstract
Summary
The effects of PGE1 and its three metabolites, 15-keto-PGE1, dihydro-PGE1, and 15-keto-dihydro-PGE1, were studied in anesthetized dogs and in isolated dog hind limb preparations. The systemic hemodynamic effects of these three metabolites were qualitatively similar to those of PGE1 in dogs, but the magnitude of the effects was smaller with these three metabolites than with PGE1. Among these metabolites, dihydro-PGE1 exerted the most potent hemodynamic and vasodilator actions. The present study suggests that the inactivation of PGE1 in the lungs is caused, not by the saturation of the Δ13 durable bond of PGE1, but by the oxidation of the secondary alcohol group at C-15 and probably by further degradation.
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