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Prostaglandin Mediates Premature Delivery in Pregnant Sheep Induced by Estradiol at 121 Days of Gestational Age

Department of Obstetrics and Gynecology (W.X.W., T.C., K.C., V.C.), University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104; Department of Obstetrics and Gynecology (J.R.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157; and Department of Obstetrics and Gynecology (P.W.N.), Center for Women’s Health Research, New York University Medical School, New York, New York 10016

Address all correspondence and requests for reprints to: Dr. Wen Xuan Wu, Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, RP1, Suite 470, 800 North Research Park, Oklahoma City, Oklahoma 73104. E-mail: wen_xuan_wu{at}hotmail.com.

The experiments reported here were designed for both in vivo and in vitro approaches in the same animals to obtain a better picture of the role of estrogen in the control of parturition. Chronically catheterized pregnant ewes were treated with vehicle (n = 5) or estradiol (n = 6), 5 mg twice a day, im for 2 d starting at d 119 of gestation. Maternal and fetal plasma estradiol, progesterone, and cortisol were measured by RIA and maternal plasma prostaglandin (PG) F2 was measured by enzyme immunoassay. Intrauterine PG H synthase 2 mRNA and protein and placental P450_c17 hydroxylase mRNA were determined by Northern, in situ hybridization, Western blot analysis, and immunocytochemistry. Data were analyzed by ANOVA.

Five of six estradiol-treated ewes delivered their fetuses within 48 h; however, the placenta was still retained 5–6 h after fetal delivery. Both maternal plasma estradiol and PGF2 increased significantly in the estradiol-treated group. Maternal and fetal plasma progesterone and cortisol were not altered in either group. There were significant increases of PGH synthase 2 mRNA and protein in myometrium, endometrium, and maternal placenta but not in fetal placenta in estradiol-treated ewes. Placental P450_c17 hydroxylase mRNA was not detectable in vehicle or estradiol-treated groups.

Estradiol can, in the absence of increase in plasma cortisol, stimulate uterine PG production and induce labor, resulting in fetal delivery in the sheep. Failure of placental delivery after estradiol treatment suggests that estradiol alone is insufficient to stimulate some of the key changes required to complete delivery at the stage of gestation studied.

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