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Effects of bovine follicular fluid and exogenous oestradiol on the GnRH-induced short luteal phase in anoestrous ewes

The role of oestradiol in the control of premature luteolysis (previously shown to occur by the normal luteolytic mechanism involving PGF₂ and oxytocin) was investigated in anoestrous ewes induced to ovulate using GnRH (250 ng every 2 h for 24 h followed by 125 µg on day 0) without progesterone pretreatment. Seven ewes were administered charcoal stripped bovine follicular fluid (bFF) on days 1–5 (2 ml by s.c. injection every 8 h) together with oestradiol on days 2–4 (4 µg in 1 ml of corn oil by i.m. injection every 8 h). Ten ewes were treated with bFF and corn oil (as above), and ten ewes received saline and corn oil (control group). All ewes were treated with 1 µg oxytocin (i.v.) on day 4 and plasma was collected for measurement of 13,14-dihydro-15-keto PGF₂ (PGFM). Blood samples were collected for measurement of progesterone and oestradiol (day–2 to 15). The ewes in the control group that responded to GnRH formed either normal (50% of ewes) or short-lived (50% of ewes) corpora lutea identified by progesterone profiles. The proportion of ewes that displayed premature luteolysis was reduced (P < 0.05) by bFF treatment alone (to 11% of ewes), and increased (P < 0.001) by bFF plus oestradiol treatment (to 100%). bFF treatment suppressed oestradiol concentrations (P < 0.01), whereas bFF plus oestradiol treatment increased oestradiol concentrations (P < 0.001) on days 1–5. The high oestradiol concentrations appeared to stimulate the premature luteolytic mechanism as the mean PGFM response to oxytocin was higher in the ewes treated with bFF plus oestradiol than in the other two groups (P < 0.001). In addition, the control ewes that formed short-lived corpora lutea had higher oestradiol concentrations (days 1–5) than did ewes with normal corpora lutea (P = 0.05). This study suggests that short-lifespan corpora lutea are the result of increased oestrogenic stimulation of the luteolytic mechanism during the early luteal phase (following a lack of prior exposure to progesterone) which can be overcome by suppressing oestradiol secretion. This finding demonstrates that oestradiol plays a key role in the initiation of premature luteolysis, probably through stimulation of the prostaglandin response to oxytocin.