Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ovulation Inhibition”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
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↗
PubMedDate not supplied

Tumor necrosis factor-alpha inhibits ovulation and steroidogenesis, but not prostaglandin production in the perfused rat ovary.

OBJECTIVE: We tested the null hypothesis that tumor necrosis factor-alpha (TNF-alpha) does not decrease ovulation, estradiol and progesterone production, or prostaglandin (PG) E2, PGF2alpha, or 6 keto-PGF1alpha production in the open bursa rat ovarian perfusion model. METHODS: Experimental animals were controlled for age, weight, litter, and pregnant mare's serum gonadotropin (PMSG) aliquot. Female Sprague-Dawley rats, 26-27 days old, were injected with 25 IU PMSG. Forty-eight hours later, the right ovary was dissected, the bursa removed, and the specimen placed in the perfusion chamber with defined media. Luteinizing hormone and isobutylmethylxanthine were given as an ovulatory trigger. Test perfusions also received TNF-alpha in 0.8-nmol/L, -pmol/L, and -fmol/L doses. Samples were collected at 0, 1, 3, 5, 7, 10, and 20 hours. Ovulations were counted at 20 hours. Steroids and PGs were measured. RESULTS: The addition of TNF-alpha to the rat ovarian perfusion model resulted in a dose-dependent decrease in ovulations (mean +/- standard deviation): 16.14 +/- 6.2 in controls (n = 7) versus 2.38 +/- 3.4 with TNF-alpha 0.8 nmol/L (n = 7), and 4.3 +/- 1.5 with TNF-alpha 0.8 pmol/L (n = 3), both P < .001. Tumor necrosis factor-alpha also inhibited estradiol (P < .005) and progesterone production (P < .05) throughout, but produced no significant changes in PG production. CONCLUSIONS: Tumor necrosis factor-alpha inhibits ovulation in a dose-dependent fashion, and inhibits estradiol and progesterone production without altering PG production in the open bursa rat ovarian perfusion model.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Gonadotropin-releasing hormone (GnRH) inhibits ovulation induced with luteinizing hormone (LH) in proestrous hypophysectomized rats.

In this paper we present evidence that a single low dose of the natural synthetic gonadotropin-releasing hormone (GnRH), inhibits ovulation induced by LH in proestrous-hypophysectomized rats. Rats hypophysectomized by the parapharyngeal route in the morning of proestrus received an intravenous injection of 100 or 300 ng GnRH at 1400 h immediately followed by 1.0 microgram LH per 100 g bw. In control groups, either one or both hormones were replaced with 0.9% NaCl. Ovulation was assessed the following morning by counting the ova present in oviductal flushings. All the rats treated with LH alone ovulated, and the addition of GnRH reduced significantly the number of ovulating rats and the number of ova per ovulating rat. In other groups of rats hypophysectomized in the morning of proestrus and treated in the same way, ovarian or adrenal secretory rates of estradiol and/or progesterone were measured after cannulation of the corresponding vein, in the afternoon of proestrus. In these animals, GnRH failed to inhibit either the ovarian progesterone surge observed 2 h after LH administration, or the adrenal progesterone secretion. All hypophysectomized rats showed lower ovarian secretory rate of estradiol than intact rats; this rate was not affected by treatment with LH or LH plus GnRH. The systemic estradiol levels in plasma of hypophysectomized rats were distributed within a range of 20 pg/ml to 50 pg/ml. The number of rats whose levels were above 21 pg/ml on estrus day was significantly higher in rats receiving 300 ng GnRH as compared to those receiving 100 ng GnRH, reaching values that surpassed the concentration found in intact, untreated animals at the same time of estrus. This effect did not depend on LH administration.

Adrenal Glands↗
PubMed1983

Antagonists of the luteinizing hormone releasing hormone with pyridyl-alanines which completely inhibit ovulation at nanogram dosage.

[N-Ac-D-2-Nal1,pCl-D-Phe2,D-3-Pal3,D-Arg6,D-Ala10]-LHRH caused 100% and 57% inhibition of ovulation in rats, s.c., at 500 and 250 ng, respectively, and 56%, per os at 500 micrograms. [N-Ac-3,4-diC1-D-Phe1,pC1-D-Phe2,D-3-Pal3,D-Arg6,D-Ala10]-LHRH inhibited ovulation, s.c., 82% at 500 ng, and 63%, per os at 500 micrograms. These analogs are the most effective reported inhibitors of ovulation. The new introduction of pyridyl-alanines can be superior substituents. For pairs of analogs, relationships are: D-3-Pal (beta-(3-pyridyl)-D-alpha-alanine) in position 3 is superior to D-Trp3, D-2-Pal3 and D-4-Pal3. D-Arg6 was superior to D-3-Pal6 and D-4-Pal6 was superior by 2-fold to D-Arg6. D-Ala10 was superior to Gly10 and D-Abu10.

Alanine↗
PubMed1995

RU486 inhibits ovulation, fertilization and early embryonic development in rabbits: in vivo and in vitro studies.

OBJECTIVE: To clarify the role of P in ovulation, fertilization, and early embryonic development using RU486, a potent P receptor blocker. DESIGN: Ovulatory efficiency, IVF, and early embryonic development were evaluated after RU486 administration in vivo and in vitro. SETTING: Research laboratory of a university hospital. PARTICIPANTS: Mature male and female New Zealand white rabbits. INTERVENTIONS: Animals were treated with RU486 or vehicle for 3 days before hCG-induced ovulation. Ovaries treated with hCG to induce ovulation were perfused for 6 hours in vitro with RU486 or vehicle. In vitro fertilization was performed in the presence or absence of RU486. MAIN OUTCOME MEASURES: The percentage of mature follicles ovulating (ovulatory efficiency) was determined after in vivo and in vitro treatment. Fertilization, morula, and blastocyst development were evaluated every 24 hours for 120 hours. RESULTS: RU486 significantly inhibited ovulation, fertilization, and early embryonic development. CONCLUSIONS: Progesterone plays a significant role in ovulation, fertilization, and preimplantation embryonic development.

Animals↗
PubMedDate not supplied

[The effect of oral ovulation inhibiting (mono-, bi- and triphase) contraceptives and of Continuin and Postinor on proteo- and steroid hormones].

Endocrinological changes due to the effect of treatment with mono-, bi- and three-phase contraceptive pills taking continuously and occasionally are reviewed. It is established that oral contraceptives based on ovulation inhibition are safe. Less side effects are produced by Ovidon tablets. Continuin and Postinor pills are not safe, and they can produce irregular bleeding. Beside their numerous advances extrauterine pregnancy frequently happens (6.4%). A three-phase preparation is expected to have a reversible effect and lack of a consequent functional infertility. This is improved by hormone level measurements.

Adult↗
PubMed1993

The angiotensin II antagonist saralasin inhibits ovulation in the perfused rat ovary.

OBJECTIVE: Our null hypothesis was that the angiotensin II antagonist saralasin does not reduce the number of ovulations in the rat ovarian perfusion model. STUDY DESIGN: Ovaries from pregnant mare's serum gonadotropin-stimulated immature rats were perfused with nutrient media to which luteinizing hormone and 3-isobutyl-1-methylxanthine had been added to induce ovulation. Test perfusions were treated with saralasin 1 mumol/L (n = 0.5) and compared with controls (n = 5) with the Student t test. Perfusions with both saralasin and angiotensin II and dose-response evaluations were performed. RESULTS: Saralasin-treated ovulations were 6.6 +/- 1.3 (mean + SEM) compared with 18.6 +/- 3.9, p < 0.02. The effects of saralasin could be reversed with the addition of an equimolar amount of angiotensin II. Dose-response evaluations showed a progressive inhibition of ovulation at 10(-8) to 10(-6) mol/L. CONCLUSION: The angiotensin II antagonist saralasin inhibits ovulation in a dose-dependent fashion; this effect is canceled by the addition of equimolar concentrations of angiotensin II.

Angiotensin II↗
PubMed1975

Progesterone: sites of action in inhibiting ovulation in hamsters.

A single subcutaneous injection of progesterone (0.5 mg/animal at 17.00 hours) on Day 3 of the cycle (Day 1 = day of vaginal discharge) interfered with ovulation and external vaginal discharge in all the animals. Lower doses were only partly active. Intravenous administration of LH, FSH or their combination at 14.00 hours on Day 4 failed to restore ovulation in such animals, implying a direct action of the administered progesterone on the ovary. A large dose of oestradiol benzoate (400 mug/animal) also proved inactive suggesting that progesterone did not interfere with ovulation solely through antioestrogenic action. Depletion of the pituitary LH stores normally found in association with ovulation and ovulatory peak of LH in plasma seen in control animals were not observed in the progesterone-treated hamsters suggesting a further action of progesterone at the pituitary-hypothalamic level in inhibiting ovulation. Administration of synthetic LRF (100 ng/animal, i.v.) on Day 4 to hamsters treated with progesterone caused an increase in plasma LH 15 min later which was comparable to the rise observed in control animals given a similar injection of LH-RF, implying lack of action of progesterone at the pituitary level. It is concluded that progesterone acts centrally, principally on the hypothalamus, and peripherally on the ovary to interfere with ovulation in hamsters. It is possible that the anovulatory state accompanying pregnancy results from these actions.

Animals↗
PubMed1975

Ovulation inhibition with human chorionic gonadotrophin.

Eight women with regular menstrual cycles were treated daily during 9 cycles with HCG (Human Chorionic Gonadotrophin) 3000 or 5000 IU daily for a period of 4-7 days. This treatment was started between the 1st and the 6th day after the onset of menstruation. Control of the treatment cycles was performed by basal body temperature, pregnanediol serial estimations, endometrial biopsies and in addition in 5 treatment cycles by radio-immunological assay of estradiol-17 beta (Oe2), progesterone, LH and FSH from the serum at intervals of 1 to 3 days. In 6 of these cycles where treatment started on the 4th day or later, ovulation was inhibited (2 cycles) or postponed (4 cycles) to the 24th-46th day. In these 6 treatment cycles the progesterone and pregnanediol increase during HCG treatment was poor or absent. The typical Oe2 increase of the normal menstrual cycle was impaired. In the 3 remaining cycles where treatment was started on the 1st, 2nd and 4th day, we observed during HCG treatment increases in Oe2 and progesterone serum values similar to that found during corpus luteum activity, and menstruation from a secretory endometrium between the 13th-19th day of the cycle. The histologically examined ovaries of one woman who was treated with HCG from the 2nd to the 6th day of the cycle showed distinct luteinization of the theca interna of all tertiary follicles and a beginning degeneration of the granulosa. These findings give support to the hypothesis that the luteinization of the theca interna leads to degeneration of the tertiary follicles thereby causing ovulation inhibition or postponent of ovulation.

Adult↗
PubMed1986

[Inhibition of ovulation with 35 micrograms of ethinyl estradiol and 2 mg of cyproterone acetate (Diane 35)].

In the study reported here the ovulation inhibition dose for cyproterone acetate was determined. Experiments showed that the ovulation inhibition dose is 1 mg of cyproterone acetate, administered daily. Results proved that the cyproterone acetate dose cannot be reduced when cyproterone acetate is combined with ethinyl estradiol. However, the objective of this study was to determine whether it is possible to reduce the estrogen dose to 35 micrograms when the common combination of 2 mg cyproterone acetate and ethinyl estradiol is being used. After a control menstruation cycle, 2 mg cyproterone acetate and 35 micrograms ethinyl estradiol were administered daily to six women with normal menstruation. Drug administration began on Day 5 and ended on Day 25. During the control cycle, the first treatment cycle, and the third treatment cycle, LH, FSH, 17 beta estradiol, progesterone, testosterone, prolactin, and SHGB were examined daily. Cervix score and karyopyknosis index were determined at the same time. In addition, antithrombin III was examined during the control cycle and during the third treatment cycle. Present results show that ovulation inhibition is possible with dose reduction of ethinyl estradiol to 35 micrograms, combined with 2 mg of cyproterone acetate. Increase in SHBG and reduction in testosterone serum level point to an additional antiandrogenic effect of cyproterone acetate, aside from its cellular effect. The combined preparation discussed here does not bring about any changes in antithrombin III values. Results permit the conclusion that ovulation inhibition is insured with a reduction of the daily estrogen dose from 50 micrograms to 35 micrograms.

Adult↗
PubMed1982

Long-lasting ovulation inhibition with a new injectable progestagen ORG-2154.

A new long-acting injectable progestagen was tested in 15 women who volunteered for the study. The occurrence of ovulation was assumed by the elevation of progesterone levels above 2ng/ml following a pre-ovulatory estradiol peak. Following a 200mg injection, ovulation was inhibited in all 15 women for five to ten months. In four subjects the interval between the injection and the first progesterone peak was five months. For eight, the interval was six to eight months. In the other three women, ovulation occurred more than eight months following injection. Bleeding episodes, similar to menstruation, occurred in most patients. Bleeding intervals lasting longer than 45 days occurred in nine subjects but more prolonged amenorrhea lasting longer than 60 days was reported by only five subjects. Blood chemistry which included blood cell counts, cholesterol, glucose, alkaline phosphatase, transaminases, urea nitrogen and creatinine remained within normal limits throughout the treatment.

Adult↗