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Inadequate function of corpora lutea following the induction of ovulation with monensin and FSH in seasonally anoestrous ewes

Atkinson, S. (1988) Inadequate function of corpora lutea following the induction of ovulation with monensin and FSH in seasonally anoestrous ewes. Journal of Endocrinology, 117 (2). pp. 167-172.

Link to Published Version: http://dx.doi.org/10.1677/joe.0.1170167
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Abstract

Sixteen ewes in mid-seasonal anoestrus were stimulated to ovulate using sequential injections of FSH (total dose 10 mg) over a 4-day period. Half of the ewes received a dietary growth promotant (monensin) known to enhance the ovarian response to exogenous gonadotrophins. The ewes were ovariectomized on day 5 or 11 (day 0 = the initiation of FSH treatment). Serial blood samples were taken in half of the ewes to determine peripheral concentrations of LH and a single sample of ovarian venous blood was collected before ovariectomy. All luteal structures were dissected from the ovaries, counted and incubated in vitro to determine progesterone production. The luteal structures were then examined histologically for the abundance of luteal cells.

The physical appearance of the ovary, along with plasma concentrations of LH and ovarian venous oestradiol indicated that the monensin-treated ewes ovulated before control ewes. The corpora lutea from control ewes produced significantly (P <0·05) more progesterone than did the corpora lutea from the monensin-treated group. Furthermore, only 7% of the remaining luteal structures in the monensin-treated group produced significant amounts of progesterone on day 11, whereas 61% of the luteal structures in the control group were actively secreting progesterone. The mean number of granulosa cells in the follicles was similar at ovulation in the two groups, but the mean numbers of large and small luteal cells were significantly (P <0·05) lower in luteal structures from the monensin-treated ewes than in those from the control ewes. It is therefore postulated that inadequate corpora lutea function following precocious ovulation is due to a lack of luteal cell development formed after premature luteinization.

Publication Type: Journal Article
Murdoch Affiliation: School of Veterinary Studies
Publisher: Society for Endocrinology
URI: http://researchrepository.murdoch.edu.au/id/eprint/34261
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