Maintenance of Corpora Lutea and Pregnancy in Hypophysectomized Rabbits

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Abstract
Hypophysectomy during the 2nd week of gestation resulted in severe follicular involution and degeneration of the corpora lutea (CL). Within 7 days, no progesterone could be detected in the ovarian effluent, and implant sites were the only remaining evidence of pregnancy. Degeneration of the interstitial tissue (LST) was less evident; although little or no basal 20[alpha]-hydroxypregn-4-en-3-one (20[alpha]-OH) secretion was measurable, substantial amounts of this steroid (but no progesterone) were secreted following acute LH [luteinizing hormone] stimulation. None of the pituitary gonadotrophins (LH, FSH [follicle-stimulating hormone], or prolactin) supported luteal function when administered individually, but each one exerted a specific effect on ovarian structure and function: LH, in doses of 150 or 250 [mu]g x 2 daily sc [subcutaneous], depleted IST cholesterol and induced ovarian atrophy; FSH, 200-500 [mu]gx2 daily sc, stimulated follicular growth; and prolactin, 500 [mu]g x 2 daily sc, produced IST hypertrophy. When prolactin was combined with FSH (either with or without 5-20 [mu]g of LH), progesterone secretion was partially maintained and pregnancy terminated less quickly. On the other hand, estradiol benzoate (EB), 2 [mu]g in 95% sesame oil; 5% beeswax x 2 daily sc, sustained luteal morphology and progesterone secretion and maintained pregnancy in 50% of the hypophysectomized animals. When EB was combined with prolactin, hypertrophy of both luteal tissue and IST was evident and ovarian weight was comparable to that of intact, pregnant controls. These data indicate that estrogen exerts a direct, trophic effect on the CL and that prolactin and FSH are essential for estrogen secretion in the rabbit. Since prolactin induces IST hypertrophy and FSH promotes follicular growth, both the IST and the follicle appear to have positive role in regulating estrogen production.