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Results for “Luteolytic Effects”

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At least 325 records · Page 18Linked to original sources
PubMed1981

Anovulatory effect of a LHRH antagonist in women.

The antagonistic analog of LHRH, NAc-D-p-Cl-Phe(1),(2), D-Trp(3),D-Phe(6), D-Ala(10)-LHRH was administered intramuscularly in a dose of 2 mg to ten normally ovulating women on day 12 of the menstrual cycle. Ovulation was inhibited in six patients, and two more presented an insufficient corpus luteum. No pregnancies were recorded in this series. In those patients who did not ovulate, it was demonstrated that the LHRH analog abolished the midcycle surge of both LH and FSH. Luteolysis evidenced by the rapid decline in progesterone levels was present in 2 cases. Bleeding pattern showed a tendency to delayed menses. The morphological findings in endometrial biopsies of 6 women exhibited mild proliferation. Further research along these lines is necessary for appraisal of this approach to birth control.

Adult↗
PubMed1984

Luteinizing hormone-releasing hormone (LHRH) and its analogs for contraception in women: a review.

In animals, LHRH agonists have multiple sites of action including the pituitary, the gonads, and the reproductive tract. In humans, the major antifertility action of this class of peptides is believed to be mediated via the pituitary. Studies in women have indicated that potent LHRH agonists can block ovulation when administered once daily. In the volunteers who have used these agents no serious side effects were observed, although some women experienced irregular bleeding or amenorrhea. It is anticipated that formal clinical trials could be conducted in the near future to determine the efficacy of continuous LHRH agonist administration. Early attempts to use an LHRH agonist to produce luteal insufficiency, luteolysis, or interruption of pregnancy have either been unsuccessful or the results are still too preliminary to ascertain whether these approaches warrant further trials. LHRH antagonists are believed to act by inhibiting the action of LHRH on the pituitary. Although some of these peptides are known to be active in women, very large doses have been required. Recently several investigators have produced LHRH antagonists with increased potency. In the near future, it should be possible to determine whether these peptides should be considered as potential contraceptives in men or in women.

Abortion, Induced↗
PubMed1975

Action of prostaglandin F2alpha on pregnancy in hamsters: luteolytic and extra-ovarian effects.

Pregnancies in hamsters may be terminated by 10 mug PGF2alpha administered b.i.d. on days 4, k and 6 of gestation. Small (250 mug and above) daily injections of progesterone on the same days will reverse this PG effect; in contradistinction, 10 mg of progesterone per day failed to maintain normal pregnancies in hamsters spayed on day 5. Daily administration of 3 mg of progesterone and 1 mug of estrone essentially normalized the gestation; administration of PGF2alpha at 10 mg on days 5, 6 and 7 of pregnancy in steroid-maintained rats, resulted in pregnancy termination in all animals, while 1 mg was partly effective. These data demonstrate an extra-ovarian site of action of prostaglandin F2alpha on pregnancy in hamsters.

Animals↗
PubMed1993

Hydrogen peroxide evokes antisteroidogenic and antigonadotropic actions in human granulosa luteal cells.

The nature of the luteolysin in humans is unknown. Hydrogen peroxide (H2O2), notably released by activated leukocytes, is generated in the rat corpus luteum at luteolysis and evokes luteolytic-like effects in rat luteal cells. We, therefore, evaluated the actions of H2O2 in human luteinized granulosa cells. After 2 days of preculture with low levels of hCG, human granulosa luteal cells were placed in suspension culture for 1 h in the presence of isobutylmethylxanthine (100 microM). A 60-min challenge with hCG evoked dose-dependent stimulation of cAMP and progesterone production. H2O2 dose-dependently inhibited progesterone production (ED50, 50-100 microM) in the absence or presence of hCG and blocked hCG-stimulated cAMP accumulation. Inhibition of progesterone synthesis by H2O2 was near maximal within 5 min, whereas inhibition of cAMP accumulation was not evident until 60 min. Cell viability was unaffected by H2O2, and inhibition of cAMP was reversible, but inhibition of steroidogenesis was long-lasting. Progesterone production stimulated by 8-bromo-cAMP, 22-hydroxycholesterol, and pregnenolone was inhibited by H2O2 as was androstenedione-dependent estradiol production. These findings indicate that H2O2 blocked progesterone synthesis by inhibition of cholesterol side-chain cleavage cytochrome P450, 3 beta-hydroxysteroid dehydrogenase, aromatase, and/or 17 beta-hydroxysteroid dehydrogenase. While H2O2 blocked stimulation of cAMP accumulation in response to hCG and cholera toxin, this same response produced by forskolin or aluminum fluoride was unaffected by H2O2. Thus, H2O2 appears to uncouple LH (hCG) receptors by interruption of G-protein-dependent activation of adenylate cyclase. In summary, H2O2 evokes effects in isolated human granulosa luteal cells that are associated with luteal regression, which raises the interesting possibility that H2O2 may serve a role as a mediator of this process like that in the rat.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

[Luteal insufficiency and benign breast diseases. Study in the light of data from the combined LH-RH + TRH test together with the study of ovarian steroids].

Luteal deficiency has been attributed a patho-physiologic role in benign fibro-cystic breast disease, whereas Prolactin would not be involved in this disease. To tes these hypotheses, patients with fibro-cystic breast disease have been investigated through the combined LH-RH + TRH test, coupled with ovarian steroids estimations. 63 menstruating patients with ovulatory cycles, as evidenced by the temperature curve and proven fibro-cystic breast disease, as demonstrated by senography and thermogrphy and/or operation, have been selected for this study. The findings do not favour the role of luteal dificiency but rather the role of PRL hyperactivity in the pathol-physiology of fibro-cySTIC BREAST DISEASE.

Breast Diseases↗