Dk. Vanderwall et al., CORPUS LUTEAL FUNCTION IN NONPREGNANT MARES FOLLOWING INTRAUTERINE ADMINISTRATION OF PROSTAGLANDIN E(2) OR ESTRADIOL-17-BETA, Theriogenology, 42(7), 1994, pp. 1069-1083
The objective of this study was to test the hypothesis that intrauteri
ne administration of prostaglandin E(2) (PGE(2)) or estradiol-17 beta
(E-17 beta) would prolong CL function in nonpregnant mares. Nonpregnan
t mares were continuously infused with 240 mu g/d of PGE(2), 6 mu g/d
of E-17 beta, or vehicle (sham-treated) on Days 10 to 16 post ovulatio
n (ovulation = Day 0), using osmotic minipumps surgically placed into
the uterine lumen on Day 10 (n = 11 per group). Nonpregnant and pregna
nt mares served as negative and positive controls, respectively (n = 1
1 per group). Mares were defined as having prolonged CL function if pl
asma progesterone remained >2.5 ng/ml and if ovulation did not occur o
n Days 9 to 30. Corpus luteal function was prolonged until Day 30 in 1
/11 nonpregnant mares, 4/11 sham-treated mares, 6/11 E-17 beta-treated
mares, 8/11 PGE(2)-treated mares, and 11/11 pregnant mares. The incid
ence of prolonged CL function was similar (P=0.16) in the sham-treated
and nonpregnant mares. The hypothesis that PGE(2) would prolong CL fu
nction in nonpregnant mares was supported, since the incidence of prol
onged CL function was higher (P=0.003) in PGE(2)-treated versus nonpre
gnant mares, tended to be higher (P=0.09) in PGE(2)-versus sham-treate
d mares, and was not lower (P=0.11) in PGE(2)-treated versus pregnant
mares. The hypothesis that E-17 beta would prolong CL function in nonp
regnant mares was not supported, since the incidence of prolonged CL f
unction was not higher (P=0.34) in E-17 beta-versus sham-treated mares
, and was lower (P=0.02) in E-17 beta-treated versus pregnant mares. T
hese results demonstrate that intrauterine administration of a pharmac
ologic dose of PGE(2) initiated prolonged CL function in nonpregnant m
ares. Further experiments are needed to confirm the role of conceptus
secretion of PGE(2) in CL maintenance, and to determine the mechanism
of action of PGE(2) within the equine reproductive tract.