Key result
PGE1 metabolites exert weaker hemodynamic and vasodilator effects than PGE1, with dihydro-PGE1 being most potent.
Why the study?
The systemic hemodynamic effects and inactivation mechanisms of PGE1 metabolites in dogs were not fully characterized.
Answers are grounded in this paper and cite their sources.
The study suggests that the inactivation of PGE1 in the lungs is caused by the oxidation of the secondary alcohol group at C-15 rather than the saturation of the Δ13 double bond.
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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Jiro Nakano (1971) studied this question. PGE1 and its metabolites (15-keto-PGE1, dihydro-PGE1, and 15-keto-dihydro-PGE1) vs. PGE1 was evaluated on Systemic hemodynamic effects and vasodilator actions. The systemic hemodynamic effects of PGE1 metabolites were qualitatively similar but smaller in magnitude than PGE1, with dihydro-PGE1 exerting the most potent hemodynamic and vasodilator actions.
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