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Results for “Luteolytic Effects”

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PubMed1993

Effects of oxytocin and uterine and luteal prostaglandins on the functional regression of the corpus luteum in pseudopregnant rats.

The effects of oxytocin on luteal regression in the pseudopregnant rat and whether the luteolytic effect of oxytocin could be blocked by an oxytocin receptor antagonist were investigated. We determined the temporal relationship between the effects of oxytocin on the duration of pseudopregnancy and concentrations of progesterone in plasma, and uterine and luteal prostaglandin concentrations. Pseudopregnancy was induced in normal cyclic rats by gonadotrophin treatment. On day 6 of pseudopregnancy, rats were assigned to one of three groups. One group was given oxytocin, 500 mU s.c., twice a day for three days. A control group was given saline injections. A third group was given the same dose of oxytocin and an oxytocin receptor antagonist, [Pen1,Phe(Me)2,Thr4,Orn8]oxytocin, 300 micrograms day-1, delivered by micro-osmotic pumps for the same three-day period. Rats were either observed to determine the duration of pseudopregnancy, or killed on days 2, 6, 7, 9, 11 and 13 of pseudopregnancy for measurements of plasma concentrations of progesterone and luteal and uterine PGF2 alpha and PGE2 concentrations by radioimmunoassays. Oxytocin injections shortened the duration of pseudopregnancy from the mean of 13.5 +/- 0.3 days for the control group to 11.5 +/- 0.3 days for the oxytocin-treated group (P < 0.01). The oxytocin-induced shortening of pseudopregnancy was associated with a premature functional regression of the corpus luteum. Both luteal and uterine PGF2 alpha concentrations were found to increase with luteolysis and reached peak values before the return of oestrus. However, only uterine PGF2 alpha synthesis was stimulated by oxytocin treatment. There was no significant increase in uterine or luteal PGE2 synthesis during luteolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1975

Induction by PGF2a of 20alpha-hydroxysteroid dehydrogenase in first generation corpora lutea of the rat.

20alpha-Hydroxysteroid dehydrogenase (20alpha-OH-SDH) activity was determined in the first generation corpora lutea from prepubertal rats injected with 10 I.U. of pregnant mare's serum gonadotrophin (PMSG) on day 30. The enzyme was not detectable in 1-9-day-old corpora lutea but a significant activity was seen on day 10. Enzyme activity increased during day 11 and day 12. In vivo administration of prostaglandin F2a (PGF2a) induced the enzyme in rats with corpora lutea older than 3 days. When prolactin was given concurrently with PGF2a, the corpus luteum activity of 20alpha-OH-SDH was lower than when PGF2a was given alone. It is concluded that the present "corpus luteum model" is suitable for further analysis of the cellular mechanisms of the luteolytic effect of prostaglandins (PGs) as well as of the role of gonadotrophins in the luteolytic process.

Animals↗

PubMed2003

Nitric oxide as a local mediator of prostaglandin F2alpha-induced regression in bovine corpus luteum: an in vivo study.

To test whether nitric oxide (NO) is involved in prostaglandin (PG) F2alpha-induced regression of the bovine corpus luteum (CL) in vivo, heifers were treated as follows: Group 1, saline (3 ml/h); Group 2, dinoprost, an analogue of prostaglandin F2alpha (aPGF2alpha; 5 mg/0.5 h); Group III, Nomega-nitro-L-arginine methyl ester (L-NAME; 200 mg/4 h), an inhibitor of nitric oxide synthase; and Group IV, L-NAME (400 mg/4 h) and aPGF2alpha (5 mg/0.5 h). All treatments were administered by an intraluteal microdialysis system (MDS) on day 15 of the cycle. Perfusate and jugular plasma samples were collected at half-hour intervals; additionally, jugular plasma samples were collected once daily from day 16 to day 21 of the cycle. In the perfusate samples, aPGF2alpha increased P4 (P < 0.05), PGE2 (P < 0.001), and LTC4 (P < 0.05) concentrations; L-NAME increased P4 (P < 0.05) but did not change PGE2 and LTC4 (P > 0.05) concentrations as compared with the period before treatment. Simultaneous perfusion of CL with L-NAME and aPGF2alpha caused a further increase of P4 concentration (P < 0.05) induced by L-NAME or aPGF2alpha treatment and increased PGE2 and LTC4 (P < 0.001) concentrations to the level observed after aPGF2alpha treatment. Perfusion of CL with aPGF2alpha caused luteal regression within 24 h, while perfusion with L-NAME prolonged the life span of CL to day 21 (P < 0.05). Concomitant L-NAME and aPGF2alpha treatment partially counteracted (P < 0.05) the luteal regression caused by aPGF2alpha administration. These results show that NO is involved in the process of luteolysis in the bovine CL and suggest that the luteolytic effect of aPGF2alpha may be mediated by NO as an important component of an autocrine/paracrine luteolytic cascade.

Animals↗

PubMedDate not supplied

The value of progesterone, oestradiol benzoate and cloprostenol in controlling the timing of oestrus and ovulation in dairy cows and allowing successful fixed-time insemination.

The relative merits of three hormone treatments of dairy cows: (1) intravaginally administered progesterone and oestradiol benzoate; (2) intravaginally administered progesterone and injected cloprostenol; and (3) injected cloprostenol; begun 35-75 days after calving and designed to synchronize oestrus and ovulation and allow successful artificial insemination (AI) at fixed times, have been assessed utilizing information from progesterone concentrations in milk. From this it was concluded that 89% of the cows had ovulated one to three times between calving and the beginning of treatment. Treatment (2) was more effective than (1) in synchronizing ovulation. This was due to the fact that when treatments began early in the ovulation cycle, the requirement for a rapidly effective luteolytic agent was provided by cloprostenol but not by oestradiol benzoate. Treatment (2) was also more effective than (3) in synchronizing ovulation. This is interpreted as meaning that progesterone treatment for 12 days had a beneficial effect in restoring normal cyclic ovarian function in the cows after calving. Whilst cloprostenol administered alone did not have this beneficial effect, there is no evidence that it had a detrimental effect. Based on all cows in treatment groups, the proportion that became pregnant to the fixed-time AI was significantly greater after treatment (2) than after (1), but when based on numbers of cows with synchronized ovulation, there were no significant differences among treatments in the proportions becoming pregnant. The progesterone/cloprostenol treatment had a disadvantage in that when begun during the 11-22 day period of the ovulation cycle, so resulting in a long, total period of suppression of ovulation (mean, 32.1 days), fertility to the fixed-time AI was poor despite effective synchronization of ovulation. Ovulation cycles immediately following the failed, fixed-time AI were normal, both in length and in maximum, luteal-phase progesterone concentration and indicated normal corpus luteum function. Thus the infertility could be ascribed neither to poor timing of AI nor to gross degeneration of follicles prior to their synchronized ovulation following the prolonged suppression of ovulation. The 12-day progesterone treatments when given to anovulatory cows gave, within 5.5 h of their beginning, a concentration of progesterone in milk that was not significantly different from the maximum reached. This concentration declined during the 12 days of the treatment but remained above pretreatment level until 5.5 h after treatment withdrawal; the maximum reached was about half that in normal ovulation cycles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1979

Comparison of the lytic effects of four prostaglandin analogues in the chacma baboon (Papio ursinus ursinus).

Six healthy, cycling female chacma baboons (Papio ursinus ursinus) were used to determine the luteolytic effects of four prostaglandin analogues. The compounds were administered according to a study design which made provision for adequate controls. Five to seven days following ovulation, venous blood was collected and the baboon given a single intramuscular injection of a compound at a recommended dose. Blood was then collected serially every 3 h for three samples and again at 24, 48, and 72 h to determine the continued effect of the prostaglandin analogues on corpus luteum production of progesterone. It was found that PGF2alpha-1,15-lactone, 11alpha(15S)-17-phenyl-18,19,20-trinor-ent-PGE2 methyl ester and 17-phenyl-18,19,20-trinor-PGF2alpha exhibited definite luteolytic potential in this species. Equivocal results were obtained with (15S)-15-methyl-PGF2Alpha THAM and its toxic qualities resulted in the demise of three animals.

Animals↗

PubMed1990

Reproductive hormones during termination of early pregnancy with mifepristone.

Thirteen women received a single oral dose of 600 mg mifepristone (RU486; Roussel-Uclaf, Paris, France) on day 0 to induce first-trimester abortion. Eleven women had a complete abortion, and 2 had a continuing pregnancy and were considered as failures. Plasma levels of human chorionic gonadotropin (hCG) increased from day 0 in all women, but dropped sharply after day 3 in women with successfully induced abortion. In these women, the levels of progesterone, 17 alpha-hydroxyprogesterone and estradiol-17 beta increased from day 0 to day 1 and then dropped. In the 2 failed inductions, the steroid levels remained virtually unchanged. In the complete abortions, the main prostaglandin F2 alpha metabolite, 15-keto-13,14-dihydro-PGF2 alpha, increased to a significant peak at day 6 followed by a significant fall to day 14. These findings supports a direct effect of mifepristone on the decidua, initiating prostaglandin synthesis. It is also suggested that there is a luteolytic effect of prostaglandin F2 alpha, as the levels of corpus luteum steroids started to fall before the drop in hCG.

17-alpha-Hydroxyprogesterone↗

PubMed1978

In vivo effects of antisera to prolactin receptors in female rats.

Antisera generated in guinea pigs against partially purified PRL receptors derived from rabbit mammary glands were tested for their effect on PRL binding and the biological effects of PRL in vitro and in vivo. Several dilutions of either normal guinea pig serum or anti-PRL receptor serum were incubated in vitro with homogenates of rat ovaries. Although specific binding of PRL was inhibited as much as 90% by the anti-serum, normal guinea pig serum had little effect. There was no inhibition of binding of LH and FSH to ovaries by these antisera. When these antisera were administered to normal cycling rats, the most pronounced effect was an increase in the number of corpora lutea, presumably due to the prevention of the luteolytic effect of PRL. When one of these antisera was given to adult rats immediately after parturition, weight gain of their pups decreased significantly, possibly reflecting a decrease of milk yield. Thus, passive immunization of animals with anti-PRL receptor sera modifies the actions of PRL on some of its target tissues.

Animals↗

PubMed1975

Effects of prostaglandin f2a on ovarian blood flow and vascular resistance in the pseudopregnant rabbit.

In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2a. The measurements were performed on days 5-10 of pseudopregnancy induced by 500 IU HCG iv.

Animals↗

PubMed1981

A receptive period for estradiol-induced luteolysis in the rhesus monkey.

This study was performed to test the hypothesis that responsiveness to the luteolytic action of estradiol is acquired as the luteal phase of the menstrual cycle progresses. The luteolytic effect of fixed estradiol increment (270 +/- 12 pg/ml serum) was assessed at different stages of luteal function in rhesus monkeys. A 4-day elevation in estradiol early in the luteal phase (days 2--6 after the LH peak) caused a decrease in the concentration of serum progesterone but did not shorten luteal life span. In contrast, when provided during the midluteal phase (days 6--10), the same 4-day estradiol increment promptly induced premature luteolysis. Furthermore, during sustained exposure to the extradiol increment from days 2--10, signs of premature luteolysis were not evident until day 7 after the LH peak. Thus, the effects of estradiol early in the luteal phase do not alter luteal life span; it is the effects after day 6 that precipitate luteolysis. These observations support the existence of a receptive period for the luteolytic action of estradiol in the rhesus monkey.

Animals↗

PubMed1983

The effect of prolactin pretreatment on prostaglandin F2 alpha-associated structural changes in membranes from rat corpora lutea.

The ability of prolactin treatment to antagonize the luteolytic effect of prostaglandin F2 alpha (PGF2 alpha) was examined in the rat. Animals were superovulated, treated with PGF2 alpha and various doses of prolactin. Plasma progesterone concentrations were measured to assess luteal function. Microsomes were prepared from ovarian homogenates and examined by wide-angle x-ray diffraction for evidence of structural changes in the cellular membranes during luteolysis. In addition, the concentrations of various lipids were analyzed for alterations in membrane lipid composition. In preparations from control animals, all of the membrane lipid was in the liquid-crystalline phase at body temperature. However, in samples from PGF2 alpha-treated rats, portions of the bilayer underwent a structural alteration from liquid-crystalline to gel phase. This phase transition was not accompanied by significant changes in the relative concentrations of various lipids. Prolactin treatment was effective in inhibiting this membrane breakdown in a dose-dependent manner. These results suggest that PGF2 alpha and prolactin may control luteal function by affecting membrane structure.

Animals↗

PubMed1984

Studies on the luteolytic activity of MDL-646, a new gastroprotective PGE1 analogue, in the hamster.

MDL-646, 11,15-dihydroxy-16-methyl-16-methoxy-9-oxo- prost -13-en-1-oic acid methyl ester, is one of the most active members of a new class of PGE1 analogues with potent gastric cytoprotective and antisecretory activity. The potential luteolytic activities of MDL-646 and its corresponding PGE2 derivative, L 14224 were assessed from their ability to terminate pregnancy and to reduce plasma progesterone levels in the hamster. PGE1 and PGE2 were used as reference compounds. The biological and biochemical data clearly demonstrate that these 16-methyl-16-methoxy PGE derivatives, given s.c. or p.o. either once or for 3 days, have no luteolytic effects up to a daily dose of 2-2.5 mg/kg, and are therefore at most 1/2 to 1/4 as luteolytic as the parent natural PGEs. The dissociation between gastroprotective and luteolytic activity was interpreted to indicate that these new PGE derivatives have a specific action.

Abortion, Spontaneous↗

PubMed1984

Luteolytic influence of intrauterine dead embryos in the early pregnant rat.

The present investigation was an endeavour to study if annihilation of embryos in the uterus of the rat before the establishment of placental luteotropic functions has any influence on corpus luteal function, and, if there is any, whether it is local or systemic. The responsibility of pregnancy maintenance was imposed on a single ovary by performing unilateral ovariectomy after implantation (on Day 5 postcoitum). The implantation sites in one uterine horn, either ipsilateral or contralateral to the remaining ovary, were selectively destroyed by injecting 0.1 ml of sterile normal saline to that particular horn only, and the peripheral progesterone level and viability of the embryos in the untreated horn, which depended on the functions of the remaining ovary, were examined. Selective killing of embryos in the uterine horn of the ovariectomized side did not exert any influence on the fetal viability in the untreated horn ( nonovariectomized side) and the peripheral progesterone level also remained statistically unaffected. On the contrary, induction of fetal resorptions in the uterine horn of the intact side produced a significant fall in the peripheral level of progesterone and induced resorption of embryos of the ovariectomized side also. The latter could significantly be prevented by simultaneous administration of exogenous progesterone, indicating luteolysis as the major, if not sole, factor responsible for fetal resorption in the untreated horn. The luteolytic effect was attributed neither to saline itself, nor to the distension of the uterine horn caused by saline injection. Luteolytic factors from the dead embryo-bearing horn which act locally on the adjacent ovary only, are discussed.

Animals↗

PubMed1993

Effects of individual and combined treatment with prostaglandins E2 and F2 alpha on progesterone secretion by ovine luteal cells supplemented with homologous serum lipoproteins in vitro.

Prostaglandin F2 alpha (PGF2 alpha) is a potent luteolysin, whereas prostaglandin E2 (PGE2) is generally luteotropic in vivo. To establish a model system for investigations of the mechanisms involved in these actions, we examined the effects of individual and combined treatment with PGE2 and PGF2 alpha on basal and ovine LH-stimulated progesterone secretion during long-term incubations conducted with and without supplemental homologous low-density lipoprotein (LDL) as substrate. Effects of both PGF2 and PGF2 alpha were concentration- and time-dependent and were further influenced by the presence of LDL and/or LH in medium. Neither of the prostaglandins exerted any significant effect before 48 h in culture, but distinctly different patterns of response to PGE2 and PGF2 alpha emerged thereafter. Low, but not high, concentrations of PGE2 increased progesterone secretion in the absence of LH, whereas PGF2 alpha (alone and in combination with PGE2) inhibited progesterone production in all medium formulations. The transcriptional inhibitor actinomycin effectively blocked the actions of PGF2 alpha, but had no effect on response to LH or PGE2. These data demonstrate that both the putative luteotropic actions of PGE2 and the potent, luteolytic effects of PGF2 alpha in vivo can be reproduced in long-term cultures of ovine luteal cells in vitro, and they suggest that the mechanism of PGF2 alpha-induced luteolysis may involve new protein synthesis.

Animals↗

PubMed1984

Interaction between catecholamines and prostaglandin F2 alpha in human luteolysis.

From each of 14 women undergoing laparotomy at different stages of the luteal phase of the cycle, the corpus luteum (CL) was excised, cut into pieces and incubated for 120 min. Incubations were performed in the absence and presence of hCG and prostaglandin F2 alpha (PGF2 alpha). In addition, noradrenaline (NA) was added to the incubation medium of newly formed CL, and the adrenergic blocker propranolol to incubated specimens of mid-luteal phase CL. After incubation the tissue levels of protein and cyclic AMP (cAMP) and the media concentrations of progesterone (P) were determined. In young CL, PGF2 alpha did not interfere with the stimulatory effect of hCG on neither cAMP nor P formation, while in CL of the mid-luteal phase PGF2 alpha significantly counteracted the stimulatory effect of hCG on these two parameters. In the presence of propranolol, however, this antigonadotrophic effect of PGF2 alpha in vitro was abolished. Furthermore, when NA was added to specimens of young CL, PGF2 alpha significantly counteracted the stimulatory effect of hCG on both cAMP and P formation. These in vitro data show that endogenous catecholamines may regulate the antigonadotrophic, 'luteolytic' effect of PGF2 alpha in human CL.

Chorionic Gonadotropin↗

PubMed1988

Evidence for luteotrophic and antiluteolytic actions of prolactin in rats with 5-day oestrous cycles.

Injection of 1 mg bromocriptine at either 08.00 or 16.00 h on the day of oestrus in rats with 5-day oestrous cycles caused a reduction in the duration of progesterone secretion by the corpus luteum during dioestrous, and a shortening of the ovarian cycle by 1 day. These effects were not present when bromocriptine was injected at 08.00 h on the day of metoestrus. The effect of bromocriptine on progesterone secretion by the corpus luteum was reversed by neutralization of the biological activity of LH at dioestrus by injection of 0.5 ml anti-LH serum at 08.00 h at metoestrus. Injection of the antiserum alone prolonged progesterone secretion by the corpus luteum, but had no effect on the length of dioestrus. These results are interpreted as suggesting (1) that prolactin secretion on the afternoon of oestrus protects the corpus luteum of the rat ovarian cycle against the luteolytic effects of LH secretion during early dioestrus and (2) that prolactin stimulates progesterone secretion in the absence of such a luteolytic action. This response of the corpus luteum of the rat ovarian reproductive cycle to prolactin results in 5-day oestrous cycles.

Animals↗

PubMed2001

Luteal expression of cytochrome P450 side-chain cleavage, steroidogenic acute regulatory protein, 3beta-hydroxysteroid dehydrogenase, and 20alpha-hydroxysteroid dehydrogenase genes in late pregnant rats: effect of luteinizing hormone and RU486.

A decrease in serum progesterone at the end of pregnancy is essential for the induction of parturition in rats. We have previously demonstrated that LH participates in this process through: 1) inhibiting 3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity and 2) stimulating progesterone catabolism by inducing 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) activity. The objective of this investigation was to determine the effect of LH and progesterone on the luteal expression of the steroidogenic acute regulatory protein (StAR), cytochrome P450 side-chain cleavage (P450(scc)), 3beta-HSD, and 20alpha-HSD genes. Gene expression was analyzed by Northern blot analysis 24 and 48 h after administration of LH or vehicle on Day 19 of pregnancy. StAR and 3beta-HSD mRNA levels were lower in LH-treated rats than in rats administered with vehicle at both time points studied. P450(scc) mRNA levels were unaffected by LH. The 20alpha-HSD mRNA levels were not different between LH and control rats 24 h after treatment; however, greater expression of 20alpha-HSD, with respect to controls, was observed in LH-treated rats 48 h after treatment. Luteal progesterone content dropped in LH-treated rats at both time points studied, whereas serum progesterone decreased after 48 h only. In a second set of experiments, the anti-progesterone RU486 was injected intrabursally on Day 20 of pregnancy. RU486 had no effect on 3beta-HSD or P450(scc) expression but increased 20alpha-HSD mRNA levels after 8 h treatment. In conclusion, the luteolytic effect of LH is mediated by a drop in StAR and 3beta-HSD expression without effect on P450(scc) expression. We also provide the first in vivo evidence indicating that a decrease in luteal progesterone content may be an essential step toward the induction of 20alpha-HSD expression at the end of pregnancy in rats.

20-Hydroxysteroid Dehydrogenases↗

PubMed1997

Effect of disruption versus continuation of gonadotrophin-releasing agonist after human chorionic gonadotrophin administration on corpus luteum function in patients undergoing ovulation induction for in-vitro fertilization.

Previous studies have described the luteolytic effect of gonadotrophin-releasing hormone agonist (GnRHa) administered in the early luteal phase. The present work was undertaken to compare in a prospective and randomized design the effect of disruption versus continuation of daily GnRHa after human chorionic gonadotrophin (HCG) administration on corpus luteum function in patients undergoing ovulation induction for in-vitro fertilization (IVF). Two different studies were designed and a total of 38 ovum donors, aged 23-30 years, were included. In the first study, the effect of GnRHa on the early luteal phase of IVF-stimulated cycles was investigated (n = 27); the patients were divided into two groups, according to whether they stopped (n = 13) or continued with daily GnRHa injections (n = 14) for an additional period of 15 days after HCG administration. Blood was drawn from luteal phase days 2 to 6 (day 0 = day of HCG administration) and oestradiol and progesterone concentrations were analysed. The second study focused on the effects of continuation versus disruption of GnRHa administration in the mid-late luteal phase. A similar design was employed including six patients who stopped GnRH on day 0 and five other women who continued GnRHa for 15 days after HCG administration. In this second study, blood was drawn from days 5 to 11 and oestradiol, progesterone and luteinizing hormone (LH) concentrations were analysed. IVF parameters were similar in both groups. The results indicate that continuous GnRHa administration, after HCG injection, does not produce changes in oestradiol, progesterone and LH concentrations in the early, mid- and late luteal phases compared to those patients in whom GnRHa is discontinued at the day of HCG administration. The present work demonstrates that, when ovulation induction is performed, the corpus luteum is driven primarily by the HCG, regardless of the administration or disruption of GnRHa in the luteal phase. This suggests that the lack of differences between continuation versus disruption of GnRHa may be due to the accumulation of the product over the previous 2-3 weeks of treatment.

Adult↗

PubMed1985

Effect of bromocriptine on prostacyclin release and cyclic nucleotides on rat aortic and uterine tissues.

The effect of bromocriptine mesylate on cyclic nucleotides and PGI2 release by rat aortic and uterine tissues was investigated. Treatment of rats with bromocriptine (10 mg kg-1 I.P. daily for 14 days) increased PGI2 release by the thoracic aorta from 0.67 +/- 0.02 to 1.4 +/- 0.03 ng/mg wet tissue (P less than 0.001; n = 6). This increase was antagonized by treatment with sulpiride (15 mg kg-l). Incubation of the arterial tissue with bromocriptine (50 micrograms ml-1) in vitro also stimulated PGI2 release. Mepacrine (160 micrograms ml-1) significantly decreased both basal and stimulated PGI2 release. Incubation of myometrial tissue from pregnant rats with bromocriptine (50 micrograms ml-1) in vitro significantly decreased PGI2 release from 1.25 +/- 0.07 to 0.60 +/- 0.08 ng/mg wet tissue (P less than 0.05, n = 6). It also elevated uterine cAMP from 40 +/- 2 to 64 +/- 3 pmoles/100 mg wet tissue. Both effects were antagonized by sulpiride. Bromocriptine did not affect uterine cGMP or the cyclic nucleotides in the aorta. It is concluded that the increase in aortic PGI2 was mediated via activation of dopamine D-2 receptors that stimulate phospholipase A2 enzyme. The decrease in myometrial PGI2 release may be related to the increase in uterine cAMP resulting from activation of dopamine D-1 receptors. Previous studies suggested a role for PGI2 in implantation in the rat. The results suggest that the inhibitory effect on uterine PGI2 may underlie the reported inhibition of bromocriptine on implantation. On broad basis, the decrease in uterine PGI2 together with the reported luteolytic effect of bromocriptine point to a potential role for the compound in postcoital contraception.

Animals↗