Changes in Gonadotropins and Steroids Associated with Unilateral Ovariectomy of the Rat1

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Abstract
To study the mechanism of compensatory ovarian hypertrophy (COH) in rats, unilateral ovariectomy (ULO) or sham operations were done on the morning of metestrus, and the concentrations of LH [luteinizing hormone, FSH [follicle stimulating hormone], prolactin, progesterone, 17.beta.-estradiol and estrone were measured in serum at various times in the immediate and the 3rd subsequent estrous cycle. A series of experiments also were done to determine the source of the acute elevation of estrone and progesterone in serum after surgery and the possible role of these steroids in COH. These experiments included effects of adrenalectomy, surgical stress and dexamethasone suppression on estrone and progesterone. Estrone and progesterone also were measured in adrenal venous blood 1 h after ovariectomy. Other experiments assessed the effect of surgical stress, estradiol replacement before ULO and estradiol binding by antisera in intact rats on FSH levels at 11 or 12 h after treatment. ULO resulted in a surge of FSH lasting from the 6th-18th h after surgery. The preovulatory surge of FSH was more prolonged into the day of estrus of the 1st and 3rd subsequent cycles after ULO than after sham operations. It is proposed that the surge of FSH at 6-18 h after ULO is responsible for COH in the immediate cycle and prolongation of the preovulatory FSH surge in subsequent cycles maintains the continued COH. Elevation of LH occurred during the first 6 h and a peak of prolactin was found at 6 h after either ULO or control surgery. Neither LH nor prolactin was altered in the 3rd subsequent cycle. Therefore, LH and prolactin do not appear to be responsible for COH. Estrone and progesterone were elevated in peripheral serum and were extremely high in adrenal venous serum after surgery. Adrenalectomy or dexamethasone blockage of these steroids did not prevent the FSH surge or COH. Replacement with estradiol before ULO did not prevent the surge of FSH and binding of circulating estradiol in intact rats with antisera did not produce an elevation of FSH. It is suggested that some material of ovarian origin other than estrogen is reduced by ULO and results in a surge of FSH to produce COH.

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