Summary. Of 19 dioestrous ewes given 50 μg GnRH on Day 10 of the oestrous cycle, 15 (79%) formed corpora haemorrhagica within 2 days after injection of GnRH. After excision of the Day 10 spontaneous CL, the GnRH-induced CL were short lived when compared to spontaneous CL in saline-treated ewes (3·1 ± 0·4 vs 17·3 ± 0·3 days, respectively). Hysterectomy of ewes bearing the GnRH-induced CL prevented regression of the short-lived CL, thus extending functional lifespan ≥ 38 days. Serum concentrations of progesterone produced by the GnRH-induced CL in hysterectomized ewes were less than those observed during a comparable interval (Days 7–14) in saline-treated, non-hysterectomized ewes (2·24 ± 0·1 vs 3·67 ± 0·15 ng/ml, respectively; P ⩽ 0·001).
When GnRH was given before (5 h before) or during (5 h after) PGF-2α-induced regression of the Day 10 spontaneous CL, the GnRH-induced CL which formed were also short-lived. In contrast, when GnRH was given following (36 h after) PGF-2α-induced regression of the Day 10 spontaneous CL, the CL which formed were not different in lifespan or production of progesterone from spontaneous CL. Efforts to enhance function of the GnRH-induced subnormal CL by treating ewes with the synthetic progestagen, norgestomet, to suppress follicular development after CL formation, were unsuccessful.
We suggest that these results provide new evidence to support the hypothesis that subnormal luteal function may be the result of inadequate follicle development (i.e. the follicle needs exposure to some sequence of events characteristic of luteal regression and/or a normal follicular phase) which impairs uterine luteolytic mechanisms. These results also support the hypothesis that periovulatory determinants of normal luteal function are established between 5 and 36 h after PGF-2α-induced luteal regression.
Keywords: corpus luteum; ewes; hysterectomy; GnRH