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Department of Obstetrics and Gynecology, West Virginia University Medical Center Morgantown, West Virginia 26506
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, FSH, prolactin, progesterone, 17β-estradiol and estrone were measured in serum at various times in the immediate and the third 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. Also, estrone and progesterone 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 to 18th h after surgery. The preovulatory surge of FSH was more prolonged into the day of estrus of the first and third subsequent cycles after ULO than after sham operations. It is proposed that the surge of FSH at 6 to 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 third 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.
Footnotes
1 Supported by NIH Research Grant No. HD-07762 from the National Institute of Child Health and Human Development.
Received January 28, 1977.
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