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Endometrial Prostaglandin F Release in Vitro and Plasma 13, 14-Dihydro-15-Keto-Prostaglandin F₂ in Pigs with Luteolysis Blocked by Pregnancy, Estradiol Benzoate or Human Chorionic Gonadotropin

U.S. Department of Agriculture, Beltsville, MD 20705

Abstract

Experiments were conducted to determine: (1) whether a plasma PGF₂ metabolite, 13,14-dihydro-15-keto- PGF (PGFM), increases during luteolysis and (2) whether pregnancy or estradiol benzoate (EB) or human chorionic gonadotropin (HCG) treatment would prevent increased endometrial PGF release in vitro and increased plasma PGFM. In Exp. 1, endometrial and luteal tissue was recovered 16 days after the onset of estrus from 27 pigs (mature gilts) in four treatment groups: (1) nonpregnant (noninseminated); (2) pregnant; (3) nonpregnant, given 10 mg of EB IM on day 12 of the cycle, and (4) nonpregnant, given 1,000 IU of HCG IM on day 12 of the cycle. Duplicate samples of luteal and endometrial tissue (ca 100 mg) were incubated in Krebs Ringer bicarbonate buffer for 2 hr in (1) air at 0 C, (2) an atmosphere of 95% 0₂ :5% C0₂ at 37 C, or (3) same as (2), but with 1.3 X 10⁴ indomethacin added. Hormones were quantified by radioimmunoassay. Progesterone in plasma and progesterone release in vitro from luteal tissue collected on day 16 indicated that pregnancy, EB and HCG blocked luteolysis. PGF release from endometrial tissue incubated in vitro at 37 C was less when tissue was from pregnant and EB-treated pigs (P<.05) than when it was from nonpregnant pigs (47.1 and 36.7 vs 80.2 ng/100 mg tissue); the mean for tissue from HCG-treated pigs, 68.6 ng/100 mg tissue, was not significantly different from the means from pigs in the other treatment groups. PGF release from luteal tissue in vitro was not significantly affected by pig treatment. In Exp. 2, 15 pigs assigned to treatment groups identical to those in Exp. 1 were bled once daily from days 12 to 20 for quantification of progesterone and PGFM in plasma. Progesterone in plasma from HCG-treated pigs increased from 3 3.3 mg/ml on day 12 to 61,8 and 72.5 ng/ml on days 16 and 17, respectively (P<.05), and the means for days 16 and 17 were greater (P<.01) than those for the other treatment groups. In nonpregnant pigs, PGFM in plasma increased from 164 pg/ml on day 12 to 1,249 pg/ml on days 14 to 17, at which time progesterone concentrations were 10% of those on day 12. PGFM in plasma was lower on days 13 and 14 in pregnant and EB-treated pigs than in nonpregnant and HCG-treated pigs (P<.01). The increase in PGFM in plasma during the time corresponding to the late luteal phase in nonpregnant pigs was completely blocked by pregnancy or by EB or HCG treatment; PGFM concentration in plasma was rarely higher than 300 pg/ml in treated pigs. Estrogen treatment or pregnancy may exert an anti-luteolytic effect in pigs by reducing uterine secretion of PGF₂; this possibility is consistent with the hypothesis that estrogen secretion by blastocysts initiates the maternal recognition of pregnancy in pigs.