PREMATURE LUTEAL REGRESSION IN THE EWE

Abstract

Ewes develop a short life-span corpus luteum after the first ovulation occurring at puberty, at the beginning of the breeding season, during the postpartum period, or when ovulation is induced with hCG or GnRH during the anestrous season. These corpus luteum cause transient progesterone increases before undergoing regression 4 to 5 days after ovulation. Premature luteal regression can be prevented by hysterectomy and through the modification of PGF2a secretion suppressing follicular development, which suggests that these short-lived corpus luteum are intrinsically normal, regressing prematurely due only to premature secretion of uterine PGF2a. In ewes with a short life-span corpus luteum there is an increase in the number of oxytocin endometrial receptors starting on day 3 post-ovulation, thus triggering the start of pulsatile PGF2a release. The hormonal environment prior to ovulation is important for the programation of uterine PGF2a secretion. Thus, progestogen pretreatment before hormonal induction of ovulation in anestric ewes results in the development of luteal phases of normal length. It is possible to prevent premature luteal regression through the manipulation of the hormonal events that control the pulsatile release of PGF2a. This has been achieved through the inhibition of follicular development and estradiol release that follows the administration of an inhibin-rich fluid, such as steroid-free bovine or equine follicular fluid. This represents an opportunity for the use for reproductive purposes of those estrous cycles that would otherwise be infertile due to premature luteal regression.