The present study was designed to elucidate gonadal steroid influences on gonadotropin release and subsequent pituitary desensitization to GnRH. Sixteen women, 10 of whom were normal and 6 of whom had hypogonadism, were infused with GnRH at rates ranging from 0.313-10 micrograms/h via an indwelling iv catheter for 66 h. Blood samples obtained throughout the GnRH infusion were analyzed for LH, FSH, estradiol, and progesterone. A prompt and substantial release of gonadotropin occurred in women with ovarian failure or during the luteal phase in normal women compared with that during the follicular phase of the menstrual cycle. Thereafter, a gradual decrease in gonadotropin secretion occurred due to pituitary desensitization, which was slower in the follicular phase than in other groups. A dose-related increase in integrated LH release occurred during GnRH infusion, but this response tapered off with administration of large doses of GnRH to women with ovarian failure or during the luteal phase. In contrast, it increased linearly up to the maximum dose of GnRH in the follicular phase. These data suggest that 1) basal levels of estrogen suppress the early rapid release of gonadotropin in response to GnRH and reduce subsequent pituitary desensitization, resulting in the prolonged release of LH; 2) estrogen widens the range of dose-related increases in gonadotropin in response to GnRH; and 3) these effects of estrogen are antagonized by progesterone.
The present experiments were performed to elucidate the mechanism of the selection and maturation of a dominant follicle in women. Eight normally menstruating women undergoing myonectomy or tubal surgery volunteered for the present study. In 3 patients who were operated on Day 9-11, a visual dominant follicle was removed. The other 5 patients underwent the removal of a newly developing corpus luteum on Day 15-21. After taking 3 or 4 preoperative blood samples in the morning after their hospitalization, blood was obtained at 3 or 6 h intervals for the first 36-45 h and at 1-3 day intervals thereafter for 21-34 days. Serum FSH, LH, estradiol and progesterone were measured by radioimmunoassay. Follicleectomy was followed by a sudden drop in estradiol and a minor increase in progesterone. FSH increased for a few days and then declined. There was a drastic, but short-term increase in LH following follicleectomy which was performed before a preovulatory gonadotropin surge. A LH surge occurred 10.7 +/- 1.2 days (mean +/- S.E.) after follicular ablation followed by a luteal phase. In contrast, there was no remarkable LH release in 4 out of 5 patients who underwent luteectomy. A slightly higher level of FSH was sustained for 2-7 postoperative days. "Luteal phase" rises in estradiol and progesterone terminated promptly following luteectomy. A LH surge was observed 14.2 +/- 1.7 days after surgery followed by a luteal phase. After either type of operation, a sustained increase in FSH was followed by a gradual increase in estradiol which preceded a gonadotropin surge. These hormonal sequences resemble those seen in the normal follicular phase. The present data demonstrated that follicleectomy and luteectomy bring on some characteristic hormonal changes which may exert stimulatory or suppressive effects on the selection and maturation of a dominant follicle after the removal of a main ovarian cyclic structure culminating in ovulation at a certain interval.
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