Surge In Women Research Articles

Luteal phase serum progesterone levels after follicle aspiration with and without clomiphene citrate treatment

Peripheral serum progesterone (P) levels were studied on random days after the spontaneous luteinizing hormone (LH) surge in women who underwent follicle aspiration. Comparisons were made with ovulatory women treated with clomiphene citrate (CC) undergoing follicle aspiration and women undergoing midcycle general anesthesia and laparoscopy without follicle aspiration. There were no differences in mean P levels in the group of women who underwent follicle aspiration, compared with the group who did not. Women treated with CC showed higher P levels during the first week of the luteal phase. During the second week of the luteal phase P levels were similar, regardless of follicle aspiration alone or in combination with CC use. In the groups not using CC, more individual women had P levels less than 10 ng/ml. Follicle aspiration does not appear to reduce luteal phase P levels in groups of patients in the natural menstrual cycle or receiving CC. Some individual patients, however, appear to be at risk for lower P levels, particularly after follicle aspiration or general anesthesia, in the natural cycle.

Effects of sex steroids on the positive estrogen feedback mechanism in intact women and castrate men.

We studied the effects of prolonged testosterone treatment on ovulatory function and positive estrogen feedback in women and of prolonged estrogen priming on gonadotropin feedback in castrate men. An estrogen provocation test was carried out in 4 groups of transsexual subjects: 12 female transsexuals in their early follicular phase (days 3-5; group 1A), 8 females who had been treated with Depo-testosterone (T) for 3-6 months (group 1B), 11 men who had been castrated 3 months previously (group 2A), and 4 male castrates treated with oral estrogen for 3 months starting 3 months after castration (group 2B). The estrogen provocation test consisted of 3 GnRH tests (100 micrograms) carried out immediately before (0 h) and 44 and 92 h after an im injection of estradiol valerate (10 mg). Responses to the estrogen provocation test in women with normal menstrual cycles (group 1A) were typically female. After initial suppression at 44 h, a LH surge (positive feedback) occurred at 92 h. Pituitary responsiveness, however, was amplified both at 44 and 92 h. Prolonged T priming of women in group 1B did not inhibit the estrogen-induced LH surge, nor was the amplitude of the surge blunted. Removal of androgens and other testicular factors (group 2A) did not result in the appearance of an estrogen-induced LH surge. On the other hand, prolonged estrogen priming in male castrates (group 2B) resulted in activation of the positive feedback mechanism; a LH surge in response to the estrogen provocation occurred. The results of the present study imply that 1) contrary to an earlier suggestion, testosterone does not block or blunt the LH surge, indicating that it is probably not responsible for suppressing the LH surge in normal men; 2) testosterone can cause ovulatory failure without suppressing the LH surge in women; and 3) prolonged estrogen priming may be involved in activation of the positive feedback mechanism in humans.

Changes in plasma progesterone concentrations around the time of the luteinizing hormone surge in women superovulated for in vitro fertilization.

The purpose of the present study was to examine plasma progesterone (P4) changes around the time of the onset of the LH surge in women superovulated with clomiphene citrate and human Menopausal Gonadotrophin for in vitro fertilization (IVF). It was considered that changes in P4 levels which should be closely associated with the onset of the LH surge may be an accurate indicator for the time of oocyte recovery for IVF and that premature P4 secretion may prevent the establishment of pregnancy after embryo replacement. The plasma P4 concentrations determined at 0800, 1400, and 2100 h during the period 36 h before to 16 h after the onset of the LH surge in 72 women showed a significant diurnal variation with the nadir at 0800 h. The onset of the LH surge was detected in 51%, 32%, and 17% of patients at 0800, 1400, and 2100 h, respectively. The first significant increase in mean P4 concentrations was coincident with the onset of the LH surge at 1400 and 2100 h but because of the diurnal nadir of P4 at 0800 h, the increase in mean P4 levels was delayed until 1400 h when the LH surge began at 0800 h. Elevation of P4 concentrations from 2 to 8 nmol/liter in individual patients at 1400 and 2100 h before the onset of the LH surge did not prevent the establishment of pregnancy after embryo transfer. P4 concentrations before and after the onset of the LH surge were higher with increasing numbers of mature follicles. We conclude that changes in plasma P4 concentrations may be used to determine the time of ovulation or oocyte recovery for IVF because of their close association with the timing of the onset of the LH surge.

Induction of midcycle gonadotropin surge by ovarian steroids in women: a critical evaluation.

Despite major efforts, the roles of estradiol (E2) and progesterone (P4) as signals for triggering the midcycle gonadotropin surge in women remain incompletely defined. In the present study, a preovulatory configuration of E2 and P4 levels was achieved during the midfollicular phase of normal women and in hypogondal women (with E2 implants) by stepwise incremental infusions of E2 and P4. During the 96 h of E2 infusion alone, reproducible and concomitant surges of LH and FSH occurred after latency periods of (mean +/- SE) 58 +/- 6.9 and 68.2 +/- 2.6 h in midfollicular and hypogonadal subjects, respectively. The mean duration of the E2-induced surge was shorter for both normal midfollicular (22.7 +/- 3.9 h) and hypogonadal women (21.8 +/- 2.5 h) than is the spontaneous midcycle surge (48 h). When P4 infusion was superimposed 48 h after the initiation of E2 infusion, a LH/FSH surge that approximated the dimension of the spontaneous surge was achieved in both groups of women. For the hypogonadal women, but not midfollicular women, P4 infusion also advanced the surge onset by 14.7 h (P less than 0.001). Our data represent the first unequivocal demonstration that incremental E2 sustained for about 60 h constitutes the ovarian signal for initiating the midcycle gonadotropin surge and that a small increment of P4 secreted by the preovulatory follicle is required to establish the normal dimension of the surge. Thus, P4, although essential for creating a normal gonadotropic surge, operates by synergizing the obligatory action of E2.

Seasonal influence of diurnal rhythms in the onset of the plasma luteinizing hormone surge in women.

The time of the LH surge onset in plasma was detected in 75 human cycles. The preovulatory LH surge began between midnight and 0730 h in two thirds of the patients. According to the season of study, the LH surge began between 1030 and 2215 h in 52.4% of the spring cycles compared with 12.9% of the cycles studied during other seasons (P less than 0.001). The highest frequency of the LH surge occurrence over a 3-h time interval was 1500 +/- 1.5 h during the spring cycles (28.6%) and 0300 +/- 1.5 h (42.5%) during the other seasons. It was estimated that ovulation occurred primarily in the morning during the spring and primarily in the evening during autumn and winter.

Biological rhythm of the luteinizing hormone surge in women

Biological rhythm of the luteinizing hormone surge in women

Effects of 17 alpha-hydroxyprogesterone on luteinizing hormone release in the rat.

Our previous study, in which we measured serum17α-hydroxyprogesterone (17-OHP) every 8hr during the periovulatory phase in women, suggested that17-OHP may have a physiological role in inducing and/or facilitating LH release. Therefore, this study was designed to elucidate the possible role of 17-0HP in LH release.Experiment 1: Three weeks after ovariectomy, rats were injected subcutaneously with 20 fig of estradiol benzoate (EB) at 1200hr (day0). The administration of 2mg of progesterone (P) or 17-OHP was performed systemically at 1200hr on day3. The injection of P elicited a significant increase of serum LH 6hr later as compared to the serum levels in the control group (p<0.05), but the injection of 17-OHP failed to alter serum LH significantly.Experiment 2: Three weeks after ovariectomy, rats were injected with EB at 1200 hr. Crystalline P or17-OHP was inserted through the outer cannula into the brain at1200hr on day3. All animals bearing17-0HP implants or P implants in the diagonal band of Broca (DBB) exhibited an increase in serum LH6hr after implantation. In regard to implants in the medial preoptic area (MPO), all rats with implants of 17-OHP and 4 of 7 with implants of P exhibited an increase in serum LH, whereas both17-0HP and P implantations in the septum failed to induce an increase in serum LH.Experiment3: All rats were injected subcutaneously with 20 fig of estradiol (E2) rather than with EB. Vaginal cornification was observed in 100% at 1200hr on day 3 after the injection of EB, but in only5.5% at 1200hr on day 3 after the injections of E2. In rats with implants in the DBB or the MPO, no significant increase of serum LH was observed after implantation of 17-OHP or P.These results suggest that the sites of stimulatory feedback action of 17-OHP on LH release are similar to those of P and that the stimulatory effects of 17-OHP are synergistic with estrogen in the induction of the LH surge.Results from the present study, in conjunction with our previous observation, strongly suggest a physiological role for 17-OHP in inducing the midcycle LH surge in women.