Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Luteolytic Effects”

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 343 records · Page 19Linked to original sources
PubMed1990

Accelerated dissolution of luteal-endometrial integrity by the administration of antagonists of gonadotropin-releasing hormone and progesterone to late-luteal phase women.

Sequential blockade of gonadotropin-releasing hormone (GnRH) and progesterone (P) receptors by potent antagonists (Nal-Glu GnRH antagonist and RU486) was conducted in late-luteal phase women to develop a once-a-month birth control method by timed advancement of ongoing luteolysis and endometriolysis. Hormonal dynamics and timing of uterine bleeding during the antagonists' imposed luteal-follicular transition were compared with spontaneous (1st to 2nd) and recovery (2nd to 3rd) cycles in 10 normally cycling women. Serum luteinizing hormone (LH) and follicle-stimulating hormone levels declined (47 +/- 4.3% and 24 +/- 3.0%, respectively) by 24 hours after Nal-Glu injection, which accelerated the ongoing luteolytic process, as evidenced by more rapid declines of serum concentrations of estradiol, P, and ir-inhibin, as compared with the corresponding control cycle. This was accompanied by the prompt (16 +/- 3.2 hours after RU486) onset of a single episode of uterine bleeding, which was advanced by 2 days. Whereas the luteal phase length was foreshortened by 2 days, the subsequent follicular phase duration was prolonged by 2 days with a normal sequence of follicular maturation, LH surge, and luteal function during the recovery cycle. We conclude that the late-luteal sequential administration of antagonists of GnRH and P resulted in acceleration of the ongoing luteolytic and endometriolytic processes without functional alterations of the subsequent cycle.

Adult↗
PubMed1977

Effect of indomethacin on estrogen-induced luteolysis in the ewe.

Three groups of 6 ewes were laparotomized on day 9 of an estrous cycle (estrus = day 0) and the corporà lutea (CL) were marked with India ink. Indwelling cannulae were inserted into the uterine horn adjacent to the CL in groups 2 and 3. Group 1 was injected intramuscularly (i.m.) with corn oil twice daily on day 9. Group 2 received 750 microng 17beta-estradiol (E2) i.m. twice daily on day 9 plus intrauterine injections of indomethacin (INDO) vehicle on days 9 through 13. Group 3 received in the same estrogen treatment plus the injection of 20 mg INDO twice daily on days 9 through 13. Jugular venous samples were taken once daily on days 9 through 14 for progesterone analysis. At re-laparotmy on day 14, the ovaries were examined for new ovulations, and the ovary bearing the marked CL was removed. Results showed that E2 induced premature luteal regression as indicated by decreased CL weights and plasma progesterone levels. INDO when given in conjunction with E2 effectively blocked the luteolytic action of E2. These results suggest that the luteolytic action of E2 is mediated via increased prostaglandin secretion and release from the uterus.

Animals↗
PubMed1995

The effects of metergoline combined with PGF2alpha treatment on luteal function and gestation in pregnant bitches.

This study was designed to determine the nature of the antiluteotrophic effect of metergoline on pregnant bitches, the occurrence of clinically evident side-effects, and the efficacy of PGF(2alpha) in initiating abortion after a course of metergoline therapy. Starting on Days 18 to 20 after the onset of diestrus, 8 adult pregnant beagle bitches were treated twice daily with 0.4 to 0.5 mg/kg po metergoline for 5 d. After receiving no treatment for the next 5 d, metergoline administration was repeated for a further 3 d, followed by twice-daily intramuscular injections of dinoprost tromethamine at 250 mug/kg. There was an overall trend for the plasma progesterone concentration to decrease during the first and second course of metergoline therapy and to rise during the intervening period of no treatment. None of the bitches aborted during or after the first 5 d of metergoline administration. No side-effects were evident during the metergoline therapy. After pretreatment with metergoline a mean of 4.8 injections of PGF(2alpha) was necessary to ensure complete abortion. All abortions were rapid and uneventful, except for the usual side-effects associated with PGF(2alpha). The plasma progesterone concentration at the onset of PGF(2alpha) treatment was positively correlated to the number of PGF(2alpha) injections needed to complete the abortion process. The plasma progesterone concentration was < 8 nmol/l for several days as a result of metergoline therapy in 6 of the 8 bitches. Only 1 bitch, however, aborted before PGF(2alpha) therapy was initiated. In the other 7 bitches PGF(2alpha) appeared to be necessary for abortion. The results suggest that the effect of metergoline has to be considered incompletely luteolytic at the doses used in this study. Even prolonged suppression of luteal function in early to mid-gestation, however, did not cause abortion without the previously documented luteolytic and/or ecbolic effects of PGF(2alpha). The average interestrus interval of cycles treated with metergoline and PGF(2alpha) was shorter (mean 182.2 d, SD 7.9 d, n = 6) than expected for this group of bitches (mean 211.4 d, SD 31.5 d, n = 7).

Journal Article↗
PubMedDate not supplied

[The luteolytic action of prostaglandin F2-alpha analogues in guinea pig's ovary].

The role of prostaglandin at the level of the female genital system is multiple; they are involved in ovulation, luteolysis, contractility of the tube muscles, contraction of the gravid uterus, dilatation of the cervix. The synthetic analogous of the prostaglandin F2 alpha are utilized in a large area of treatments, for multiple purposes. The study was made on 2 lots with 10 non pregnant female guinea pig: the first lot was the witness lot and didn't receive any substance. The second lot received 100 micrograms/kg/day Isopropyl ester PGF2 alpha. The prostaglandin analogous produces vasodilating effects on the ovary blood vessels and luteolytic effects with the destruction of the ovarian follicles.

Animals↗
PubMed1988

Effects of prostaglandin F2 alpha and a gonadotropin-releasing hormone agonist on inositol phospholipid metabolism in isolated rat corpora lutea of various ages.

The sensitivity of rat corpora lutea to luteolytic agents increases with luteal age. We examined the effect of prostaglandin F2 alpha (PGF2 alpha) and [D-Ala6,Des-Gly10]GnRH ethylamide (GnRHa) on inositol phospholipid metabolism in day 2 and day 7 corpora lutea from PMSG-treated rats. Isolated corpora lutea were incubated with 32PO4 or [3H]inositol and were treated with LH, PGF2 alpha, or GnRHa. Phospholipids were purified by TLC, and the water-soluble products of phospholipase-C activity (inositol phosphates) were isolated by ion exchange chromatography. In day 2 corpora lutea, PGF2 alpha, (10 microM) and GnRHa (100 ng/ml) significantly increased 32PO4 incorporation into phosphatidic acid (PA) and phosphatidylinositol (PI), but not into other fractions. LH provoked slight increases in PA. Results were similar with 30 min of prelabeling or simultaneous addition of 32PO4 and stimulants. In other experiments, PGF2 alpha and GnRHa provoked rapid increases (1-5 min) in the accumulation of inositol mono-, bis-, and trisphosphates. LH did not significantly increase inositol phosphate accumulation, but stimulated cAMP accumulation in 2-day-old corpora lutea. Inositol phospholipid metabolism was increased in day 7 corpora lutea compared to that in day 2 corpora lutea. This increase was associated with increased incorporation of 32PO4 into PA and PI and increased accumulation of [3H]inositol phosphates. In day 7 corpora lutea, which are very sensitive to the luteolytic effect of PGF2 alpha, the PG-induced increase in PA labeling was small and inconsistent, whereas PI labeling was unaffected in 30-min incubations. GnRHa was without effect in such corpora lutea. LH, PGF2 alpha, or GnRHa did not increase inositol phosphate accumulation in 7-day-old corpora lutea. These studies demonstrate that the transformation of young (day 2) to mature (day 7) corpora lutea is associated with an increase in luteal inositol phospholipid metabolism. The results also show that PGF2 alpha and GnRHa stimulate phospholipase-C activity in young corpora lutea, but are ineffective in mature corpora lutea, and suggest that an increase in inositol phospholipid metabolism by itself is not sufficient to explain the acute luteolytic action of PGF2 alpha and GnRH in vitro. However, phospholipase-C-derived second messengers may be involved in the action of hormones that control luteal function.

Animals↗
PubMedDate not supplied

[The luteotropic and luteolytic properties of synthetic analogs of 11-deoxy-PGE1].

The luteotropic and luteolytic properties of synthetic analogues of 11-desoxy-PGE1 were studied. Compounds Nos. 1 and 2 depending on the dose exerted the opposite effect: in low doses--luteotropic, in high doses--luteolytic. Compounds Nos. 3, 4 and 5 in the whole range of doses exhibited only luteolytic properties. The ranges of doses of prostaglandin exerting the luteotropic effect depend on the structural modifications of prostaglandin molecule. The luteolytic effect of synthetic analogue No. 5 was suggested to be determined by its influence on the hypophysis through the change of contents of cyclic nucleotides and gonadotropic hormones. It was demonstrated that the luteolytic effect of compound No. 5 is realized through the central nervous system, in particular, through the hypophysis.

Alprostadil↗
PubMed1996

A study of the luteolytic mechanism of the antiprogesterone RU486 during the late-luteal phase in pseudopregnant rats.

The purpose of this study was to examine the possible mechanism through which RU486 induces luteolysis during the late-luteal phase in pseudopregnant (PSP) rats. PSP rats received a subcutaneous injection of RU486 in sesame oil (5 mg/kg body weight) or sesame oil alone once a day between day 9 and day 11 of pseudopregnancy. Serial blood samples were collected on days 5, 9, 10, 11 and 12 and assayed for progesterone content. To examine the possible action of RU486 through a uterine and/or a pituitary (prolactin-dependent) mechanism, PSP rats and chronic hysterectomized PSP rats which had been hysterectomized before PSP induction received a subcutaneous injection of RU486 in sesame oil (5 mg/kg body weight), sesame oil alone, prolactin in 50% polyvinylpyrrolidone (15 IU/day), or RU486 and prolactin once a day between day 9 and day 11 of pseudopregnancy. Serial blood samples were collected on days 5, 9, 10 and 11 and assayed for progesterone content. Blood samples were also collected at 0400 h on day 12 and used for prolactin and progesterone determinations. To examine the direct effect of RU486 on corpus luteum and/or pituitary, hysterectomized rats underwent hypophysectomy and pituitary autotransplantation on dioestrus 1 and received a subcutaneous injection of RU486 in sesame oil or sesame oil alone for 3 days between day 21 and day 23 after surgery. Serial blood samples were collected on days 10, 21, 22, 23 and 24 and assayed for progesterone and prolactin contents. In ordinary PSP rats, serum progesterone levels were significantly (P < 0.01) lower in the RU486-treated group than in the control group (9 +/- 1 vs 53 +/- 7 ng/ml; mean +/- S.E.M.) on day 11. Serum prolactin levels at 0400 h on day 12 of pseudopregnancy were significantly (P < 0.05) lower in the RU486-treated group than in the control group (16 +/- 4 vs 154 +/- 44 ng/ml; mean +/- S.E.M.). The concomitant prolactin treatment reversed the luteolytic effects of RU486 on day 11 of pseudopregnancy. In hysterectomized PSP rats, RU486 also suppressed serum prolactin levels, and the concomitant prolactin treatment again reversed the luteolytic effects of RU486. In hysterectomized rats which were hypophysectomized and pituitary autotransplanted, RU486 treatment did not induce any significant changes in serum progesterone and prolactin levels. These results indicated that RU486 induced luteolysis during the late-luteal phase in PSP rats by suppressing prolactin secretion via a hypothalamic mechanism.

Animals↗