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On the Metabolism of Prostaglandin E1 in Patients Suffering from Arterial Occlusive Disease

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Prostaglandin E1 in Atherosclerosis

Summary

During passage through the lungs, prostaglandin E1 (PGE1) is inactivated enzymatically via 15-keto-PGE1 to 13,14-dihydro-15-keto-PGE1. Since the subsequent metabolic degradation by β-oxidation and co-oxidation takes appreciably longer, the half-life of the circulating metabolite 13,14-dihydro-15-keto-PGE1 is distinctly longer than that of the active PGE1. In the presence of plasma proteins this metabolite is unstable, and it can therefore only be measured accurately after transformation into the stable bicyclic degradation product 11-deoxy-13,14-dihydro-15-keto-11,β16ξ-cyclo-PGE1. The normal plasma levels found are 20–60 pg/ml. Intra-arterial infusion of PGE1 (10 µg over a period of 30 min) leads to a significant rise in the venous and arterial levels of the PGE1 metabolite. Since PGE1 is not completely extracted during passage through the lungs, there is also a slight rise in the venous level of active PGE1. This shows that after infusion, PGE1 is rapidly inactivated by enzymatic degradation. Thus, results indicating that PGE1 infusion has a longer lasting therapeutic effect cannot be explained by a direct action of the short-lived PGE1 or 15-keto-13,14-dihydro-PGE1.

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© 1986 Springer-Verlag Berlin Heidelberg

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Simmet, T., Peskar, B.A., Wolf, H.R.D. (1986). On the Metabolism of Prostaglandin E1 in Patients Suffering from Arterial Occlusive Disease. In: Sinzinger, H., Rogatti, W. (eds) Prostaglandin E1 in Atherosclerosis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71679-9_2

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  • DOI: https://doi.org/10.1007/978-3-642-71679-9_2

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-17240-6

  • Online ISBN: 978-3-642-71679-9

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