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Department of Animal Science, University of Wyoming, Laramie, Wyoming 82071
Address all correspondence and requests for reprints to: Dr. W. J. Murdoch, Department of Animal Science, P.O. Box 3684, University of Wyoming, Laramie, Wyoming 82071. E-mail: wmurdoch{at}uwyo.edu
The purpose of this investigation was to determine whether the timing
of ovulation induction during the follicular phase is a determinant of
consequent luteal function. Ewes were treated on day 14 of the estrous
cycle with PGF2
to synchronize luteal regression and 12
or 36 h later with an ovulatory dose of GnRH. Luteal phase serum
progesterone concentrations of normal magnitude were characteristic of
animals elicited to ovulate by GnRH injection 36 h after
PGF2
treatment. Follicles stimulated at 12 h of the
induced follicular phase formed subfunctional corpora lutea that were
deficient in large steroidogenic cells. Endometrial gland development
was attenuated in ewes exhibiting luteal insufficiency. The
pathophysiology of the luteal defect was associated with a
retrospective lack of granulosal cells in preovulatory follicles not
adequately primed by estradiol. Preovulatory LH surges were not
affected by the time of GnRH treatment. Corpus luteum rescue indicative
of maternal recognition of pregnancy occurred in inseminated ewes that
were injected with GnRH 36 h after PGF2
.
Gonadotropic stimulation 12 h after PGF2
typically
resulted in gestational failure; a marginal improvement in the
pregnancy rate was attained by progesterone supplementation. We suggest
that premature induction of ovulation compromises the estrogen-mediated
succession of granulosal cell proliferative events that necessitate the
formation of a fully competent corpus luteum.
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