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At least 19 recordsLinked to original sources
PubMed1986

Ovulation inhibition by administration of weekly gonadotropin-releasing hormone antagonist.

To test the feasibility of administering the GnRH antagonist [(Ac-pClPhe1,pClPhe2,DTrp3,DArg6,DAla10) GnRH] intermittently to inhibit ovulation, this agent was given to normal ovulatory cynomolgus monkeys once weekly for 4 weeks. Ovulation was blocked in all females (eight of eight) throughout the 32 study weeks and resumed within 14.3 +/- 3.8 (+/- SEM) days in six of eight primates. Interestingly, mean tonic serum estradiol levels were not significantly reduced during treatment. Conversely, although midcycle levels of estradiol were not found, moderate estradiol levels occurred but they did not elicit preovulatory LH surges during the week after GnRH antagonist injection. In a second study directed at clarifying the mechanism(s) by which estrogen-induced LH surges were blocked, monkeys received GnRH antagonist in the early through the midfollicular phase of the menstrual cycle during which an estrogen (n = 3) or a GnRH (n = 4) challenge test was given on cycle day 6. Among monkeys receiving estradiol benzoate or a bolus dose of GnRH during the GnRH antagonist regimen, only those given GnRH (four of four monkeys) had increased LH secretion. These responses were similar to those of control monkeys (n = 3). Indeed, the pituitary was refractory (three of three monkeys) to estrogen-positive feedback for the LH surge. These findings indicate the potential utility of intermittent GnRH antagonist treatment to achieve contraception by ovulation inhibition, without creating a severely hypoestrogenic milieu attendant with the risks of negative sequelae effecting bone calcium loss, hot flushes, and atrophy of estrogen-dependent genital tissues.

Animals↗
PubMed2002

Complete and robust ovulation inhibition with NuvaRing.

NuvaRing, a novel contraceptive vaginal ring, releases 15 microgram of ethinylestradiol (EE) and 120 microgram etonogestrel (ENG) per day. A randomized pharmacokinetic study compared NuvaRing with a combined oral contraceptive (COC) containing 30 microgram EE and 150 microgram desogestrel. Maximum levels of EE and ENG with NuvaRing were 30% and 40%, respectively, of those seen with the COC. Because ENG bioavailability was higher following vaginal administration, the systemic progestogen exposures were comparable with the two contraceptives. However, the EE bioavailabilities were similar with both routes and so EE exposure with NuvaRing was half that with the COC. Pharmacodynamic studies have examined ovarian function during recommended and altered NuvaRing use. The use of NuvaRing for the recommended 3-week period completely inhibited ovulation. During an additional 2 weeks of use, ovulation continued to be inhibited. Early NuvaRing removal after just 3 days had no effect on the time to ovulation compared with recommended use, thus indicating that 3 days of use seem to be sufficient to suppress ovarian activity. Finally, delayed ring insertion (when the follicles had developed to 13 mm) resulted in inhibition of ovulation in all women. In conclusion, NuvaRing effectively inhibits ovulation during recommended and altered use, showing that it is a robust contraceptive method.

Biological Availability↗
PubMed1981

Facilitation of sexual receptivity in the rat by an ovulation-inhibiting analog of LHRH.

An LHRH analog known to inhibit ovulation in the rat ([N-Ac-Phe1, D-p-Cl-Phe2, D-Trp3,6]-LHRH) was tested for its effects on sexual receptivity. The dose of 500 ng/rat was found in dose-response experiments to be most active and was further investigated for its behavioral effects in rats treated with either estrogen or estrogen plus progesterone. The analog significantly facilitated the behavior of rats in regimens producing low [estradiol benzoate (EB) (2 microgram)] and intermediate [EB (2 microgram) plus progesterone (2.5 mg)] levels of sexual behavior. In rats given regimens producing high behavioral scores [EB (5 microgram) plus progesterone (1 mg)], the peptide did not reduce mating behavior. In the same experiment, rats given EB (5 microgram) but not progesterone showed significantly higher scores after the LHRH analog only if they had been designated "responders" by a previous screening test with 1 microgram LHRH. These results demonstrate that in animals showing low, intermediate, or high levels of sexual behavior, the LHRH analog can affect mating behavior in a direction quite different from that exerted on pituitary reproductive functions.

Animals↗
PubMed1978

The mechanism of ovulation inhibition by triamcinolone acetonide.

A single dose of 25 mg triamcinolone acetonide, when given on day 1 or 2 of the menstrual cycle, inhibits ovulation. To examine the mechanism of this action, daily determinations of plasm FSH, LH, estrone plus estradiol (E1 + E2), and progestins were performed. Some subjects also received a single dose of LH-RH or hCG on cycle day 15 or clomiphene citrate on days 5-9. Triamcinolone acetonide itself caused variable suppression of plasma estrogens, loss of the mid-cycle gonadotropin surge, and a deficient or absent rise in plasma progestins. Impaired secretion of estrogen did not seem to be due to low gonadotropin levels. FSH and LH responses to LH-RH were adequate in relation to prevailing estrogen levels. Four of six women treated with clomiphene responded with plasma progestin levels which exceed 8 ng/ml. Triamcinolone acetonide seems to affect the hypothalamic-pituitary-ovarian axis mainly by hypothalamic suppression and possibly by a direct effect on the ovary as well.

Adult↗
PubMed1987

Increased bone turnover during gonadotropin-releasing hormone superagonist-induced ovulation inhibition.

Superactive stimulatory analogs of GnRH inhibit ovulation in women. This investigation was done to assess bone turnover during GnRH agonist-induced anovulation. Particular interest was directed to the effects of smoking, since smokers have an increased risk of osteoporosis. Fasting serum calcium, phosphate, PTH, and bone Gla-protein (osteocalcin) levels, as well as urinary calcium, cAMP, and hydroxyproline excretion and the renal tubular threshold for phosphate were determined before and after 6 months of GnRH superagonist contraceptive treatment in 47 women, 22 of whom smoked more than 10 cigarettes daily. Before treatment the women who smoked had significantly higher serum phosphate concentrations and lower serum PTH concentrations than the women who did not smoke. Fasting serum calcium and the urinary calcium to creatinine ratio increased after treatment in all women, especially in the nonsmokers. The nonsmokers also had more pronounced increases in serum phosphate and osteocalcin concentrations. A decrease in serum PTH during treatment was confined to the nonsmokers. These results suggest increased bone resorption and turnover during GnRH agonist-induced anovulation and indicate that smoking habits should be taken into account in the evaluation of bone disease.

Adult↗
PubMed2001

Use of the novel combined contraceptive vaginal ring NuvaRing for ovulation inhibition.

OBJECTIVE: To assess the effects of the combined contraceptive vaginal ring NuvaRing on ovarian function. DESIGN: Randomized, open-label, crossover study. SETTING: Clinical pharmacology unit. PARTICIPANT(S): Sixteen healthy female volunteers. INTERVENTION(S): Group 1: one cycle of combined oral contraceptive containing desogestrel (150 microg) and ethinyl estradiol (30 microg) (desogestrel/EE COC), followed by a NuvaRing treatment period. Group 2: NuvaRing treatment period followed by a cycle of desogestrel/EE COC. MAIN OUTCOME MEASURE(S): Follicular diameter, serum hormone concentrations (follicle-stimulating hormone, 17beta estradiol, luteinizing hormone, and progesterone), and endometrial thickness. RESULT(S): NuvaRing use for the recommended period of 3 weeks resulted in complete inhibition of ovulation, as assessed by vaginal ultrasound (follicular diameter) and by serum luteinizing hormone and progesterone concentrations. Inhibition of ovulation was maintained for an additional 2 weeks of NuvaRing use. Ovarian suppression between the groups was comparable. Furthermore, ovarian suppression after 3 weeks of NuvaRing use was comparable to that on day 21 of DGS/EE COC intake. NuvaRing was well tolerated. CONCLUSION(S): NuvaRing completely inhibited ovulation throughout the normal 3-week period and the extended period of use. Ovarian suppression was comparable to that with desogestrel/EE COC.

Adolescent↗
PubMed1984

Ovulation inhibition in the pregnant mare's serum gonadotropin-treated immature rat: a bioassay for luteinizing hormone-releasing hormone antagonists.

A convenient method for evaluating the biological activity of luteinizing hormone-releasing hormone (LHRH) antagonists was devised. Pregnant mare's serum gonadotropin (PMSG) treatment of immature rats is known to stimulate follicular growth and estrogen production, that in turn stimulates the release of LHRH which triggers an ovulatory discharge of luteinizing hormone (LH) from the pituitary. The present bioassay of the antagonists is based on the inhibition of ovulation in the PMSG-treated rats. Twenty-eight-day-old Sprague Dawley rats maintained under a light period of 12 h/day (lights on at 0630 h) were given 10 IU of PMSG s.c. at 0930 h. On Day 30 of age the antagonist was given s.c. at 1430 h. The rats were killed on the following morning and the oviducts examined for the presence of ova. In addition, the antagonists were compared in their ability to inhibit serum testosterone levels in adult male rats. In the PMSG-treated rats the order of ovulation-inhibiting potency of the following antagonists was: [Ac-D-NAL(2)1,4FD-Phe2,D-Trp3,D-Arg6]-LHRH (LHRH-1) greater than [Ac-delta 3 Pro1,4FD-Phe2,D-NAL(2)3.6]-LHRH (LHRH-2) greater than [Ac-delta 3 Pro1,4FD-Phe2,D-Trp3,6]-LHRH (LHRH-3). The order of potency was confirmed by their antitesticular effects in adult male rats.

Animals↗
PubMed1975

Studies on the mechanism of the ovulation-inhibiting effect of 19-norsteroids in cyclic rats.

Experiments performed in cyclic female rats demonstrated an equal ovulation-inhibiting activity of the 19-norgestagens norethynodrel, lynestrenol and norethisterone acetate after injection in oestrus and metoestrus, and after daily administration from oestrus to pro-oestrus. The results furthermore show that, after application of the minimal ovulation-inhibiting doses during oestrus and metoestrus, these substances 1. induce an increase in prolactin secretion, 2., with the exception of norethisterone acetate, possess a hypophysial site of action, 3. are able to induce deciduoma formation following traumatization of the uterus, and 4. maintain the reactivity of the cyclic corpora lutea to the injection of prolactin. The findings suggest that the prolactin-releasing and luteotrophic action of the progestagens studied may form an essential part of the mechanisms that are responsible for the inhibition of ovulation observed in rats after administration over one cycle.

Animals↗
PubMed1985

Concentration-dependent mechanisms of ovulation inhibition by the progestin ST-1435.

We summarize the hormonal profiles of women at different stages of inhibition of ovarian function during sustained-release subcutaneous treatment with a progestin, ST-1435. In the highest release group of ST-1435, a decrease in the luteinizing hormone (LH)follicle-stimulating hormone (FSH) ratio was found; and in spite of follicular phase levels of plasma FSH, inhibition of folliculogenesis, as judged by plasma estradiol (E2) concentrations below 60 pg/ml, occurred during the entire treatment period of 230 days. This may be indicative of a direct action of ST-1435 on the ovaries. When the average plasma concentration of ST-1435 decreased below 100 pg/ml, follicle development had started in most of the study subjects. At that time, the LH/FSH ratio had normalized to that found during the follicular phase of the normal menstrual cycle. In spite of the E2 rise during follicular development, no midcycle gonadotropin surges or subsequent elevations in plasma progesterone concentrations were found, thus indicating that the positive feedback action of E2 on gonadotropins was blocked by this progestin. We infer that the mechanism of inhibition of ovulation by sustained parenteral treatment with the progestin ST-1435 is concentration dependent, in such a manner that lower plasma concentrations of ST-1435 act on the hypothalamus and/or pituitary, whereas at higher plasma concentrations of ST-1435, a direct effect on the ovaries is also achieved.

Adult↗
PubMed1982

Optimum time for administration of indomethacin to inhibit ovulation in the rabbit.

The antiinflammatory agent, indomethacin, inhibits ovulation in mammals by interfering with the synthesis of prostaglandins in preovulatory follicles. To determine the optimum time to administer this inhibitor, indomethacin was given at specific intervals from 10 h before, and up to 9 h after, the ovulatory process had been initiated by hCG (50 I.U./kg). The drug dosage ranged from 1.25 mg/kg to 40 mg/kg. The optimum time to give indomethacin was at 7-8 h after hCG (i.e., 2-3 h before expected rupture of the follicle) at which time the minimum effective dose was 2.5 mg/kg. Since a significant elevation in prostaglandin synthesis occurs as early as 3-5 h after hCG stimulation of rabbit follicles (1), these results reveal that nonsteroidal antiinflammatory agents can interrupt the ovulatory process even after the follicle has begun producing substantial amounts of prostaglandins. The data suggest that prostaglandins need to be produced continuously in the follicle up to the time of actual rupture or else that indomethacin is interfering with some other aspect of the ovulatory process which transpires after the elevation of prostaglandins.

Animals↗
PubMed1987

Ovulation inhibition with 17 beta-estradiol cyclo-octyl acetate and desogestrel.

Ovulation inhibition and bleeding control with a combination of 0.5 mg 17 beta-estradiol cyclo-octyl acetate (E2COA) and 0.15 mg desogestrel was investigated in 10 regularly menstruating women for 21 days. In half the group the treatment was extended for 7 days (days 22-28) with 0.03 mg desogestrel in order to evaluate any posttreatment influence on the gonadotropin levels. E2COA, beeing a long-chain fatty ester dissolved in oil, was expected to be resorbed from the intestinal wall via the lymphatic system. By incorporating it in the chylomicrons, E2COA would thereby avoid the unfavourable first liver pass. The serum levels of progesterone were suppressed during treatment. No increase in 17 beta-estradiol (E2) concentration was found; levels remained low and even during medication. No peak values of gonadotropins were seen. Thus follicular hormonal activity and ovulation was inhibited by this combination. Bleeding control was, however unacceptable in all volunteers. The addition of desogestrel during the fourth investigation week apparently did not induce any hormonal differences. The estrogenic activity is shown by the low, even S-E2 levels, but the dosage of E2COA seems to be too low in relation to progestogen dosage. Further studies will have to be performed in order to find the ideal combination.

Adult↗
PubMed1983

A study of the ovulation-inhibiting effects of dexamethasone in the domestic hen.

Laying hens were injected with a series of graded doses of dexamethasone following the terminal oviposition of a sequence to determine the effect of this compound on the time of ovulation. It was found that injection of 10-500 micrograms of dexamethasone/kg inhibited ovulation but there was no evidence of an ovulation-inducing effect when the dose was reduced below 10 micrograms/kg. The results for dexamethasone are in contrast to the effects of corticosterone which inhibits ovulation at high doses and induces ovulation at lower doses providing the hens are injected at the stage of the ovulatory cycle used in this study. It is suggested that the ovulation-inducing action of corticosterone involves a target site remote from the hypothalamic-pituitary axis.

Animals↗
PubMedDate not supplied

Ovulation-inhibiting properties of Org OD 14.

Org OD 14 has recently been shown to be an interesting new steroid for the treatment of menopausal women. In view of the importance of treatment of perimenopausal women, in whom ovulation might occur, the aim of the present study was to assess whether or not Org OD 14, administered orally in a daily dose of 2.5 mg for 21 days, inhibits ovulation. Sixteen healthy female volunteers, aged 20-34 years and with established ovulatory cycles, were studied during a control cycle and a treatment cycle. Daily measurements of the plasma levels of FSH, LH, E2, P and PRL were made. Endometrial specimens were obtained from nine of the volunteers between 23rd and 25th day of both cycles. The criteria for an ovulatory cycle were: (1) mid-cycle FSH, LH and E2 peaks; (2) criteria (1) followed by a rise in the P levels of greater than 10 ng/ml; (3) a luteal phase of at least 12 days; (4) biphasic behaviour of E2; and, (5) secretory endometrium on days 23-25 of the cycle. All control cycles were ovulatory. During the treatment the mid-cycle FSH, LH and E2 peaks disappeared, and P levels remained very low. PRL levels showed an occasional moderate rise in some of the volunteers. Endometrial specimens showed a secretory pattern during the control cycle, and different degrees of proliferation during the treatment cycle in all nine volunteers. It was concluded that Org OD 14 inhibited ovulation in all 16 volunteers.

Adult↗
PubMed1993

Interleukin-1 beta (IL-1 beta) modulates prostaglandin production and the natural IL-1 receptor antagonist inhibits ovulation in the optimally stimulated rat ovarian perfusion model.

The rat ovarian perfusion model with bursa removed and intact was used to further characterize the effects of interleukin-1 beta (IL-1 beta) and the natural IL-1 receptor anatagonist (IRAP) on ovulation, steroidogenesis, and prostaglandin production. Twenty-six- to 27-day-old female Sprague-Dawley rats were injected sc with 25 IU PMSG, and 48 h later, the right ovary was dissected (with bursa removed and intact for various experiments) and placed in the perfusion chamber. Ovaries were exposed to various doses of IL-1 beta alone, IL-1 beta with LH, and IL-1 beta with LH and isobutylmethylxanthine (IBMX). The natural IL-1 receptor antagonist was also added to the chambers with LH and IBMX. IL-1 beta at 0.8 (n = 3) and 8.0 (n = 4) nM did not induce LH-independent ovulation in PMSG-stimulated ovaries with bursa removed. In bursa-intact perfusions (n = 3), one ovulation was produced in each compared to control ovaries with bursa intact (n = 3) given an ovulatory trigger of LH alone [2.3 +/- 0.6 (+/- SD) ovulations; P < 0.02]. IL-1 beta enhanced, in a dose- and gonadotropin-dependent fashion, the production of prostaglandin E2 (PGE2) in PMSG-stimulated ovaries with bursa removed given an ovulatory trigger of LH and IBMX compared to that in controls. PGF2 alpha and 6-keto-PGF1 alpha were also modulated by IL-1 beta. Estradiol and progesterone production were not affected. The natural IRAP inhibited ovulation (7.8 +/- 3.9 ovulations vs. 12.4 +/- 1.5; P < 0.04) in PMSG-stimulated ovaries given LH and IBMX as the ovulatory trigger compared to that in controls. This inhibition of ovulation was not associated with reduced steroid or PG levels. IL-1 beta appears to play a potentially significant role in the process of ovulation. The functional importance of the bursa in this model is highlighted in this study. IL-1 beta modulates PG, but not steroid, production. IRAP inhibited ovulation without significantly affecting PG or steroid production.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Ovulation inhibition with a combined oral contraceptive containing 1 mg micronized 17 beta-estradiol.

OBJECTIVE: To evaluate ovarian function by ultrasonography and endocrine measurements. DESIGN: Prospective, open study. SETTING: Outpatient clinic of the First Department of Gynaecology and Obstetrics, University of Vienna, Austria. PARTICIPANTS: Twenty healthy women with regular cycles and established ovulation by ultrasonography. INTERVENTION: Treatment with a combination of 1 mg micronized E2 with 150 micrograms desogestrel daily for 21 days, followed by 7 pill-free days. MAIN OUTCOME MEASURES: Transvaginal ultrasonography and estimation of E2 and P at least twice a week for two consecutive cycles, followed by one after treatment cycle. RESULTS: Ovulation inhibition was apparent in all cases and no functional ovarian cysts were observed during treatment. On a few occasions a persistent follicle was noted, but in the majority of cases there was total absence of follicular activity. The bleeding pattern showed a tendency toward prolonged and more heavy bleeding when compared with the before treatment situation. Return of ovulation was prompt in all women but one. CONCLUSIONS: Ultrasonographic observations, accompanied by P and E2 measurements, allow us to conclude that the combination of 1 mg E2 with 150 micrograms desogestrel provides complete ovulation inhibition. However, the bleeding pattern does not show an acceptable profile.

Adult↗
PubMed1989

Contraceptive potential of RU 486 by ovulation inhibition: I. Pituitary versus ovarian action with blockade of estrogen-induced endometrial proliferation.

In previous studies, RU 486 administration arrested spontaneous folliculogenesis. To investigate the central versus peripheral effects of RU 486 on the ovarian/menstrual cycle, including endometrial proliferation, RU 486 was administered daily (10 mg/kg/day, im) from menstrual cycle day 3 or 7 to day 25 in normal adult cynomolgus monkeys receiving hMG treatment (37.5 IU/day) from days 3-8 (n = 6). RU 486 administration with hMG/hCG therapy did not inhibit ovarian response, as evidenced by steroidogenesis and ovulation. Nine of 23 oocytes retrieved by lavage or follicular aspiration at laparotomy after ovulation induction were morphologically classified as mature preovulatory status. Whereas an endometrial biopsy performed on cycle day 25 in control monkeys revealed an in phase mature secretory endometrium, histologic sections from RU 486 plus hMG/hCG treated females uniformly demonstrated atrophic to weakly proliferative endometrium on cycle day 25, despite serum estradiol levels greater than 300 pg/ml. Three months after the initial 25-day study endometrial biopsies revealed persistent atrophic endometrium, even though repeated ovulation induction with hMG/hCG therapy elevated serum estrogen concentrations. The findings prevailed whether RU 486 treatment began on cycle day 3 or 7. The intermenstrual interval was significantly (P less than 0.01) lengthened by RU 486 treatments (28.5 +/- 2.0, control vs 131.3 +/- 11.5 days, RU 486). In summary, RU 486 consistently blocked ovulation unless hCG was provided and elicited a persistent retardation of early proliferative endometrium when administered daily beginning in early or mid-follicular phase. The normal mitogenic effects of elevated ovarian estrogen secretion on endometrial tissue were quelled, uniformly resulting in amenorrhea. The long-lasting action of RU 486, causing ovulation inhibition and atrophic endometrium, may be due to the depot effect of im injection. In addition, RU 486 did not prevent ovarian steroidogenesis, ovulation or oocyte maturation when an ovulation induction regimen of hMG/hCG was given. These findings show that RU 486 prevented ovulation by diminishing pituitary gonadotropin secretion, rather than by direct effects on ovarian folliculogenesis, and induced amenorrhea by inhibiting estrogen-induced endometrial proliferation.

Animals↗