Effect of an OT antagonist on the control of the midcycle LH surge in women.

OBJECTIVE: Data in women regarding the role of OT in LH secretion during the LH surge are conflicting. As in previous studies blood samples for LH measurements were taken infrequently, we re-examined this matter in women with a fully characterized midcycle LH surge. DESIGN: Normal women were studied over two cycles. When the dominant follicle reached a diameter of either 16-17 mm (Group 1) or 18-19 mm (Group 2), the women were infused intravenously for 3 h with normal saline (cycle-1) or atosiban (cycle-2). PATIENTS: Fifteen women (10 in group 1 and 5 in group 2) aged 23-35 years. MEASUREMENTS: Blood samples were obtained every 6 h to characterize the midcycle LH surge. RESULTS: The time interval (mean +/- SEM) from the start of the infusion to the onset of the LH surge in the two cycles was 46.8 +/- 4.8 and 45.6 +/- 9.6 h in group 1 and 6.0 +/- 2.4 and 7.5 +/- 2.8 h, respectively, in group 2. LH values during the LH surge were similar in the two cycles except in group 1 at the point of 30 h at which LH value in cycle-2 (41.2 +/- 4.6 mIU/ml) was significantly lower than in cycle-1 (52.8 +/- 3.4 mIU/ml, P < 0.05). Nevertheless, in each group, the area under the curve for LH was similar in the two cycles. CONCLUSIONS: Antagonism of endogenous OT action by atosiban does not alter the LH profile during a fully characterized midcycle LH surge, suggesting that OT is not a major regulator of LH secretion in women.

Oxytocin is not important for the control of gonadotrophin secretion in the late follicular phase of the cycle.

OBJECTIVE: To study the role of oxytocin in basal and GnRH-induced gonadotrophin secretion in normal women. DESIGN: Normal women were studied in three cycles. When the diameter of the leading follicle was 15-16 mm, the women were infused intravenously (i.v.) for 3 h with normal saline (cycle 1), atosiban (cycle 2) or oxytocin (cycle 3). PATIENTS: The study included 12 normally cycling women aged 23-38 years. MEASUREMENTS: After cessation of treatment, two injections of GnRH, 10 microg each, were administered i.v. 2 h apart and blood samples were collected every 30 min for a total of 240 min. The 30-min pituitary response (sensitivity) to a single GnRH injection (10 microg i.v.) was investigated thereafter every 12 h from the end of the 3-h infusion until the day of LH surge onset. RESULTS: No significant differences in LH and FSH response to GnRH (sensitivity and reserve) during the 240-min experiment were found between the three cycles. The time of LH surge onset from the initiation of the infusion was similar in the three cycles. Also similar in the three cycles were oestradiol (E2) and gonadotrophin levels as well as the 30-min response to GnRH for 48 h following the 3-h infusion. CONCLUSIONS: The present study demonstrates that neither exogenous oxytocin administration nor blockage of endogenous oxytocin action influences pituitary sensitivity to GnRH in cycling women.

Alternate day and daily administration of GnRH antagonist may prevent premature luteinization to a similar extent during FSH treatment.

BACKGROUND: This randomized controlled trial was designed to evaluate whether a GnRH antagonist given every other day could prevent premature luteinization in women undergoing IVF/ICSI treatment. METHODS: A total of 73 women receiving ovulation stimulation IVF cycles with recombinant FSH were allocated randomly on cycle day 7 to GnRH antagonist ganirelix in multiple doses (0.25 mg each), either daily (n = 37 women, group 1) or every other day (n = 36 women, group 2) until the day of HCG administration. RESULTS: Serum FSH, LH, estradiol and progesterone values showed similar trends in the two groups. During FSH stimulation, 13 (35%) of the women in group 1 had premature LH rises (> or = 10 IU/l) of which eight (22%) were after the start of antagonist administration. In group 2 there were 14 (39%) LH rises during FSH stimulation of which 10 (28%) were after the start of antagonist administration. Luteinization (serum progesterone >2 ng/ml) occurred in only one woman in each group overall (3%). A significantly smaller total dose of the antagonist was used in group 2 than in group 1 (P < 0.001). The study did not have power to evaluate differences in total dose of FSH, number of oocytes recovered and clinical pregnancy rate, all of which appeared similar in the two groups. CONCLUSIONS: Whether alternate day is as effective as daily administration of ganirelix in preventing premature luteinization should be addressed in a non-inferiority trial powered to evaluate live birth rate.

Effect of follicle stimulating hormone treatment on the pituitary response to luteinizing hormone-releasing hormone in post-menopausal women.

To study the role of exogenous follicle stimulating hormone (FSH) in the attenuation of luteinizing hormone (LH) response to luteinizing hormone-releasing hormone (LHRH) during ovulation induction in women, 10 healthy post-menopausal women were treated with FSH (225 IU/day) for 5 days and normal saline (2 ml/day) for another 5 days. The two regimens were given consecutively in a 10 day experiment. The regimen for the first 5 days was randomly chosen and was given to the women in an alternate way. The response of LH to an i.v. injection of 10 micrograms LHRH was investigated twice on day 1 (i.e. before the onset of treatment and 12 h later) and once on days 2, 5 and 10 of the experiment (0900 h). Basal FSH and LH values before the onset of treatment on day 1 were similar in the five women who started with the saline and the five who started with the FSH regimen. Basal FSH values increased significantly during treatment with FSH, while LH and oestradiol values remained unchanged throughout the whole experiment. LH increment 30 min post-LHRH did not change significantly either during the first 24 h or during the whole experiment regardless of the starting regimen. These results demonstrate that in post-menopausal women the response of LH to LHRH is not affected by exogenous administration of FSH. It is suggested that exogenous FSH does not show activities on gonadotrophin secretion similar to those ascribed to a gonadotrophin surge attenuating factor.