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1,2,Colorado State University4, Fort Collins 80523
Abstract
The effects of pregnancy and number of corpora lutea on luteal regression induced with prostaglandin F2
(PGF2) were examined in 93 ewes. Bred and nonpregnant ewes were assigned randomly to receive a single im injection of PGF2: 0, 2, 4, 6, 8 or 10 mg/58 kg body weight. Injections were given on d 13 postestrus. The concentration of progesterone in serum 24 h after PGF2 injection was affected by dose (P<.001). The effect of pregnancy and the interaction of pregnancy with number of corpora lutea on levels of progesterone in serum were significant (P<.05); therefore, data were partitioned according to pregnancy status and analyzed separately. There was an effect of number of corpora lutea on serum concentration of progesterone in pregnant (P<.01) but not nonpregnant ewes (P>.10). Similar relationships among groups were observed for the concentration of progesterone in luteal tissue. In nonpregnant ewes the minimum dose of PGF2 to produce a significant suppression of progesterone in serum (P<.05) was 4 mg/58 kg body weight. In pregnant ewes with one or two corpora lutea, the minimum effective doses were 6 and 10 mg/58 kg body weight, respectively. The concentration of 13,14-dihydro-15-keto-prostaglandin F2 (PGFM) in serum was related to the dose of PGF2 injected. There were no differences in the concentration of PGFM in serum between pregnant and nonpregnant ewes either before or after injection. Corpora lutea of early pregnancy appear to be resistant to the luteolytic effect of PGF2. This effect is more pronounced in ewes with two corpora lutea. It is possible that the effect of number of corpora lutea in pregnant ewes may reflect an effect of the number of embryos (number of corpora lutea = number of embryos in 45 of 48 pregnant ewes). There is no indication that the reduced sensitivity of the corpus luteum to PGF2 during early pregnancy is due to an alteration in metabolism of PGF2.
1 Supported by a grant from the Colorado State Univ. Exp. Sta.
2 The authors wish to thank Dr. Alan Brash, Dept. of Pharmacol., Vanderbilt Univ. School of Medicine for the quantification of PGFM in serum samples by gas chromatography-gas spectrometry. The research done by Dr. Brash was supported by NIH Grant HD05797.
3 Supported by NIH Training Grant HD07031.
4 Dept. of Physiol. and Biophys.
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