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La prostaglandine E1: Donnees physiologiques et pharmacologiques
Prostaglandin E1: Physiological and pharmacological data
Andrologie volume 1, pages 126–127 (1991)
Abstract
Prostaglandins (PGs) discovered in 1930 are derived from prostanoic acid and are present in the prostate and seminal vesicles. Every tissue is capable of producing PGs from cell membranes by the action of cyclooxygenase on arachidonic acid. The half-life of PGs is very short, being less than five minutes Prostaglandin E1 or PGE1 (Alprostadil: Prostine VR, Upjohn: C20H34O5) exerts a powerful vasodilatory effect upon peripheral arteries as well as stimulating intestinal and uterine smooth muscle. A strong vasodilatory effect has also been demonstrated in vitro on cavernosal arteries and erectile tissue, via antagonism of adrenergic receptors, by Hedlund and Anderson. PEG1 which is biosynthesised in the corpus cavernosum, is metabolised by the liver, Kidneys and lungs, and destroyed by prostaglandin dehydrogenase. The first therapeutic trial of PEG1 for organic impotence was reported by Ishii in 1986, since which time many groups, especially in Europe, have reported large clinical series. This review considers the experience of some of these workers.
Resume
Les PROSTAGLANDINES ont été découvertes en 1930. Elles dérivent de l’acide prostanoïque et sont présentes dans la prostate et les vésicules séminales. Elles sont produites à partir des membranes cellulaires de tous les tissus, par action de la cyclo-oxygénase sur l’acide arachidonique. Leur durée de vie est inférieure à 6 minutes. La PGE1 ou ALPROSTADIL (PROSTINE VR® — Upjohn) a un effet vaso-dilatateur très puissant sur les artères caverneuses et le tissu érectile: c’est un antagoniste des récepteurs adrénergiques. Elle est métabolisée dans le foie, le rein et le poumon, et détruite par la 15 OH PROSTAGLANDINE DESHYDROGE NASE. Le premier essai en clinique humaine dans l’impuissance organique a été rapporté par ISHII en 1986.
References
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Etcheverry, M. La prostaglandine E1: Donnees physiologiques et pharmacologiques. Androl. 1, 126–127 (1991). https://doi.org/10.1007/BF03034266
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DOI: https://doi.org/10.1007/BF03034266