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  • Title: The effect of oxytocin and betamimetic stimulation on prostaglandin release in perfused human fetal placenta.
    Author: Ekblad U.
    Journal: Eur J Obstet Gynecol Reprod Biol; 1986 Nov; 23(3-4):153-8. PubMed ID: 3469120.
    Abstract:
    The existing data on prostaglandins indicate that they are involved in human parturition and regulation of fetoplacental blood flow. The interference of endogenous and exogenous oxytocin and prostaglandins and, on the other hand, betamimetics, which are commonly used during pregnancy, in the regulation of these phenomena is poorly understood. The production of prostaglandins by fetal placental cotyledons was studied using an in vitro perfusion technique. Isolated cotyledons were perfused without (control) or with oxytocin (200 pg/ml, 2000 pg/ml) or the betasympathomimetic drug ritodrine (10 micrograms/ml, 50 micrograms/ml). The release of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2) was measured by radioimmunoassay. The release of prostaglandins was also studied during a recovery period after the drug infusion. Oxytocin at a concentration of 200 pg/ml significantly decreased the release of PGF2 alpha. A higher concentration of oxytocin did not cause any changes in prostaglandin production. During ritodrine infusion the perfusion pressure was decreased, but the addition of ritodrine to the perfusion medium had no effect on prostaglandin release. During the recovery period, after ritodrine infusion, the release of PGF2 alpha was significantly decreased. It is suggested that oxytocin at the physiological concentration may protect the fetus from adverse effects of PGF2 alpha before labor in decreasing the release of PGF2 alpha, yet this small decrease in formation of PGF2 alpha is obviously of minor clinical importance because the perfusion pressure remained constant. Ritodrine had no effect on prostaglandin release and so the decrease in the perfusion pressure is probably the result of beta 2-receptor stimulation.
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