Attempts to improve the function of GnRH-induced corpora lutea in early post-partum ewes through oestradiol and/or PMSG priming or exogenous luteotrophin

Abstract

In order to investigate whether subnormal luteal function following induction of ovulation with gonadotrophin releasing hormone (GnRH) could be counteracted by appropriate stimulation before or after ovulation, S.A. Mutton Merino ewes ( n=65) in early lactation were induced to ovulate using GnRH at a time when subnormal luteal function was likely to result. In two experiments the ewes were infused with physiological saline (SRFS), pregnant mare serum gonadotrophin (PMSG) prior to (PRFS), PMSG after (SRFP), PMSG prior to and after (PRFP) or with PMSG plus oestradiol (E 2) prior to (EPRFS) a single injection of GnRH. A group of spontaneously cycling ewes (CYC) was used to characterize normal luteal function. At laparotomy on day 15 (experiment 1) or day 11 (experiment 2) a higher incidence (83.9%) of macroscopically active corpora lutea occurred in the ewes treated with PMSG prior to GnRH (PRFS+PRFP) than where saline was infused (65.5%) at this time (SRFP+SRFS). Of the 56 ewes which completed the experiments only five showed a short cycle of approximately 6 days, while in a further 14 ewes the cycle length approached 12 days. Of the progesterone profiles 37.2% were judged to be inadequate. In both experiments, ewes which did not receive gonadotrophin, SRFS, exhibited a progesterone profile which differed ( P<0.01) from the pooled response of those infused with PMSG. The provision of luteotrophin after GnRH was superior to PMSG priming ( P<0.01) in augmenting progesterone secretion. In experiment 2 PMSG priming improved luteal function so that it equalled that of spontaneously cycling ewes while infusion of oestradiol in addition to PMSG priming further improved luteal function ( P<0.05). The pre-ovulatory LH release was reduced ( P<0.01) by PMSG infusion before and after GnRH (not significant in experiment 1). Tonic LH levels showed that PMSG infusion raised the endogenous release of assayable LH ( P<0.05).