Abstract

Vehicle or 8 or 16 mg of PGF 2α per 58 kg body weight was given intramuscularly to intact, hysterectomized or ovariectomized 90–100 day pregnant ewes in three separate experiments. Both doses of PGF 2α increased PGF 2α in ovarian venous plasma compared with controls at 72 hr post treatment in intact (P≤0.05) but did not in hysterectomized (P≥0.05) 90–100 day pregnant ewes. Concentrations of PGE in ovarian venous blood of intact ewes did not differ (P≥0.05) between treatment groups and were equivalent to concentrations of PGE determined in uterine venous plasma. PGE was decreased in ovarian venous plasma by PGF 2α in hysterectomized ewes (P≤0.07). PGE in uterine venous plasma averaged 6 ng/ml over the 72-hr treatment period in intact and ovariectomized 90–100 day pregnant ewes and was 12 fold greater (P≤0.05) than PGF 2α which averaged 500 pg/ml in uterine venous plasma. Both PGF 2α and PGE increased (P≤0.05) by 64 hr in uterine venous plasma of the 8 mg PGF 2α — treated intact pregnant ewes. A significant quadratic increase (P≤0.05) was observed for PGF 2α and PGE in the vehicle and both PGF 2α treatment groups of intact ewes at the end of the 72-hr sampling period. It is concluded that the uterus and ovaries secrete significant quantities of PGE but little PGF 2α during midgestation. In addition, PGF 2α increased uterine secretion of PGE in vivo . PGE may be a placental stimulator of ovine placental secretion of progesterone or PGE may protect placental steroidogenesis from actions of PGF 2α.

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