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Effect of Estrogens on Uterine Tone and Life Span of the Corpus Luteum in Mares^1,2,

University of Wisconsin, Madison 53706

Abstract

The role of estrogens in development of tense uterine tone and persistence of the corpus luteum which occur in early pregnant and pseudopregnant mares was studied. The compressed thickness of the cranial end of a uterine horn increased (P<.05) between days 10 and 50 post-ovulation in pregnant pony mares. In nonpregnant, ovarian intact mares, daily (days 10 to 60) administration of progesterone (P₄) (100 mg/day) did not increase (P>.05) thickness over the day 10 (diestrus) value. Similar P₄ treatment in ovariectomized mares increased (P<.05) thickness between days 10 and 40 and at day 50 mean thickness was not different (P>.05) from that of P₄ treated ovarian intact mares, although the mean for each group at day 50 was less (P<.05) than the mean for pregnant mares. In another experiment, P₄ (100 mg/day), . 25 mg estradiol-17β (E₂) + P₄, or. 5 mg E₂ + P₄ was given daily for 50 days to seasonally anovulatory mares. Uterine thickness in P₄ and .25 mg E₂ + P₄ treated mares increased gradually until the end of treatment and then decreased, but values for .25 mg E₂+P₄ mares were not greater (P>.05) than those for P₄ treated mares. Thickness in mares treated with .5 mg E₂ + P₄ was greater (P<.05) by day 30 than for all other groups.

Treatment (days 7 to 18) with E₂ (5mg/day) or estrone (100 mg/day) appeared to lengthen and diethylstilbesterol (DES, 5 mg/day) lengthened (P<.05) the interovulatory interval over that of E₂ (.5 mg/day) or vehicle. The DES treatment caused significant luteal maintenance on day 18 as indicated by color and diameter and tended (P<.10) to cause increased luteal weight.

Results support the hypothesis that estrogens play a role in the tense uterine tone and luteal maintenance associated with pregnancy and pseudopregnancy in mares.

¹ From the Department of Veterinary Science, University of Wisconsin, Madison, WI 53706. Supported by the College of Agricultural and Life Sciences, University of Wisconsin, Madison and by Grant No. 6300505B,C from the Ford Foundation, and by Public Health Service Training Grant No. 5-T01-HD-00104-10. Part of these data were presented at the 69th Annu. Meet. ASAS (1977).

² The authors wish to express their appreciation to Dr. D. A. Snyder for surgical assistance.

³ Trainee of the Endocrinology-Reproductive Physiology Program, University of Wisconsin, Madison.