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Oxytocin stimulated release of PGF2α and its inhibition by a cyclooxygenase inhibitor and an oxytocin receptor antagonist from equine endometrial cultures

Uterine inflammation results in a poor uterine environment and early embryonic loss in the mare due to an inhibition of maternal recognition of pregnancy caused from increased prostaglandin F₂α (PGF₂α). Oxytocin binds to endometrial cell receptors to activate prostaglandin synthesis. An oxytocin rec...

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Bibliographic Details
Published in:Animal reproduction science 2013-06, Vol.139 (1-4), p.69-75
Main Authors: Penrod, Leah V, Allen, Ronald E, Rhoads, Michelle L, Limesand, Sean W, Arns, Mark J
Format: Article
Language:English
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Summary:Uterine inflammation results in a poor uterine environment and early embryonic loss in the mare due to an inhibition of maternal recognition of pregnancy caused from increased prostaglandin F₂α (PGF₂α). Oxytocin binds to endometrial cell receptors to activate prostaglandin synthesis. An oxytocin receptor antagonist (Atosiban) and a cyclooxygenase inhibitor (indomethacin) both decrease PGF₂α production. The aim of this study was to evaluate the in vitro effects of Atosiban and indomethacin on equine uterine prostaglandin secretion. Equine endometrial explants were harvested on day two of behavioral estrus. Endometrial explant cultures were challenged with oxytocin (250nM) and PGF₂α concentrations were measured over time. Explants were also cultured with Atosiban and indomethacin for 6h to determine the influence on PGF₂α secretion. When endometrial explants were challenged with oxytocin, PGF₂α concentrations were greater (P
ISSN:0378-4320
1873-2232
DOI:10.1016/j.anireprosci.2013.04.010