Ovarian Levels Research Articles

Silver Lining for Women with Migraines

Several observations suggest links between ovarian steroid levels and migraine headaches: Migraine is two to three times more prevalent in women than in men; most women with migraines report more headaches during menses; and migraine frequency drops during pregnancy, which is associated with sustained elevated estrogen levels. Given that estrogen exposure is associated with breast …

EFFECT OF VARIATION OF BODY WEIGHT, BODY CONDITION, LEPTIN, AND LUTEINIZING HORMONE RECEPTOR EXPRESSION IN POSTPARTUM ANOVULATION OF ZEBU COWS (Bos indicus)

Prolonged periods of anovulation postpartum negatively affect the productive efficiency of zebu cattle in Colombia. Postpartum anovulation is influenced by an interplay of complex processes (nutrition, milking and/or suckling) and the hormonal background orchestrated by, among others, LH and leptin and their receptors controlling steroidogenesis and follicular dynamics. This study seek for the relationship between body weight (BW) and body condition (BC, 1–5 scale) the time of appearance of first Dominant Follicles (DF) and the presence of leptin and LH receptors in the ovaries. Ovarian ultrasonography was performed during the postpartum period on eleven Zebu cows to monitor their follicular dynamics, when the third DF was detected, the cows were treated with LH (n=4) or saline solution (n=4) and 48h later they were ovariectomized to determine leptin and LH receptors by indirect immunofluorescence (IFI) and immunohistochemistry (IHQ). Cows that did not display DF were also ovariectomized (control, n=3). No significant effect of variation of BW and BC on the days to third DF was found. There was also a negative correlation between BW loss and daily BW loss with the time to the first and third DF. In FDLH group, 75% (3/4) of cows, ovulation was induced. In FDSS group, cows did not ovulate. The IFI studies for leptin and LH receptors detection were technically impossible due to the presence of autofluorescence that interfed the fluorochromes signals. In the IHQ studies for both receptors, was found a pattern of expression similar during the follicular development suggesting a comudulation to ovarian level, being greater in hemorrhagic bodies and dominant follicles, and minor in growing follicles, at granulosa, theca and luteinized cells levels. (poster)

ENDOTHELIN-2 (EDN2) INDUCED OVARIAN AND OVIDUCTAL CONSTRICTION VIA ENDOTHELIN RECEPTOR A (ETA) IN RATS

In the rat, expression of mRNA for END2 in granulosa cells dramatically, yet transiently, increases at the time of ovulation and antagonism of EDN2 receptor binding blocks ovulation. Because EDN2 is a potent constrictor of smooth muscle cells these results suggest that EDN2 may be a final contractile signal regulating ovulation. Our first objective was to further examine the EDN2 / receptor system in the ovary at the time of ovulation. In all experiments, follicular development was induced in immature rats by treatment with PMSG (10 IU) and the ovulatory cascade was induced 48 h later by treatment with hCG (10 IU). In Exp. 1, total ovarian concentrations of endothelin were determined at 0 and 12 h after hCG by enzyme-immunoassay. Ovarian levels of endothelin peptide were increased 7-fold at 12 h after treatment with hCG (P < 0.05), demonstrating that EDN2 peptide is produced prior to ovulation. In Exp. 2, isometric tension analysis was conducted using strips of ovarian tissue collected from PMSG/hCG primed rats at 10 h after hCG to determine which endothelin receptor subtype (ETA or ETB) is mediating the action of EDN2. An ETA (BQ123), but not ETB (BQ788), receptor antagonist inhibited EDN2-induced constriction of ovarian strips (P < 0.05), suggesting that EDN2 acts via ETA at ovulation. Our next objective was to examine the EDN2 / receptor system in the oviduct. In Exp. 3, cumulus-oocyte complexes (COCs) were isolated from the ovary 48 h after PMSG and at 12 h after hCG, and from the oviduct at 20 h after hCG. Real-time PCR analysis demonstrated the dramatic induction of EDN2 mRNA in COCs collected at 12 h after hCG (P < 0.05) but also revealed an 11-fold increase in expression of EDN2 mRNA in COCs collected at 20 h after hCG, compared to 48 h after PMSG (P < 0.05), suggesting that EDN2 produced from the ovary at ovulation and/or by the COCs within the oviduct may affect oviductal contractility and oocyte transport. In Exp. 4, isometric tension analysis using sections of the oviduct was conducted to determine whether the oviduct responds to EDN2 and if so, by which receptor subtype this effect was mediated through. Treatment with EDN2 induced a potent constriction of oviductal sections (P < 0.05) and concurrent treatment with BQ123, but not BQ788, inhibited EDN2- induced constriction. Immunohistochemical examination of sections of oviductal tissue also revealed strong staining for ETA but not ETB in the luminal mucosa of the oviduct. In conclusion, EDN2 is produced by granulosa cells at ovulation and appears to be acting through the ETA receptor subtype. EDN2 may also be produced by ovulated COCs within the oviduct. Contractile tissue in both the ovary and oviduct responded to treatment with EDN2, suggesting that in addition to the requirement for EDN2 at ovulation, EDN2-induced oviductal constriction may affect transportation of COCs to the site of fertilization. Supported by NIH P20 RR15592 and RO1 HD052684. (poster)

Role of inhibin and activin in the modulation of gonadotropin- and steroid-induced oocyte maturation in the teleost Fundulus heteroclitus

BackgroundActivin and inhibin are glycoproteins structurally related to the transforming growth factor-beta superfamily. These peptides were first described as factors that regulate the follicle-stimulating hormone (FSH) at the pituitary level. The possible role of inhibin and activin, at the ovarian level, in mediating the stimulatory actions of a Fundulus pituitary extract (FPE) and 17alpha,20beta-dihydroprogesterone (DHP) on oocyte maturation was investigated in this study.MethodsIn vitro culture of ovarian follicles and induction of oocyte maturation were carried out in 75% Leibovitz L-15 medium. Follicles or denuded oocytes were exposed to FPE, inhibin, activin, ethanol vehicle (control group), or DHP. The competence of the follicles or denuded oocytes to respond to the hormones was assessed by scoring germinal vesicle breakdown (GVBD) used as an indication of the reinitiation of meiosis or oocyte maturation. DHP level was measured by radioimmunoassay.ResultsAddition of FPE promoted the synthesis of DHP by the granulose cells of fully grown ovarian follicles and thus stimulated GVBD in the oocyte. Presence of porcine inhibin did not hinder the synthesis of DHP stimulated by FPE, although it did inhibit the subsequent GVBD in a dose-dependent manner, suggesting that the action of inhibin was at the oocyte level. Similarly to the findings with FPE, inhibin also blocked the DHP-induced GVBD in intact follicles, as well as the spontaneous and steroid-induced GVBD of denuded oocyte. Inhibin straightforwardly blocked the response to a low dose of DHP throughout the culture period, while higher doses of the steroid appeared to overcome the inhibitory effect especially at later times. In contrast to inhibin, recombinant human activin A significantly enhanced DHP-induced GVBD in a dose-dependent manner after 48 hr, although activin alone was not able to induce GVBD without the presence of the steroid.ConclusionTaking together with our previous studies that demonstrate the presence of activin/inhibin subunits in the ovary of F. heteroclitus, these in vitro findings indicate that inhibin and activin are local regulators in the teleost ovary and have opposing effects in modulating oocyte maturation.

Serum and ovarian Müllerian inhibiting substance, and their decline in reproductive aging

The objectives of this study were to identify whether there is a decline in Müllerian inhibiting substance (MIS) in the female rat during chronological aging, and to define the physiological basis of aging-related changes in MIS. The results demonstrate that there is an exponential decline in both serum and ovarian levels of MIS with increasing female age, and that the histologic origin for the reduction in serum levels of MIS is a decline in the number of small ovarian follicles expressing MIS.

Elaboration of a working model for the involvement of inhibin A as a mediator of the preovulatory rise of progesterone levels

During the final days of follicular development, exogenously administered follicle-stimulating hormone (FSH) produces a rise in serum progesterone level. The aim of the present study was to investigate the possible source and regulation of this preovulatory progesterone surge. Four sets of matching treatments with gonadotropins for in vitro fertilization and intracytoplasmic sperm injection were selected from a cohort of 953 treatments in 244 couples. Half of these four sets of treatments were selected based on the unusual course of the progesterone concentration during follicular development. The first set of 11 cycles with early termination of gonadotropin administration for prolonged coasting were compared with a set of 12 cycles with similar estradiol levels but with uninterrupted ovarian stimulation. Another set of 12 cycles with low preovulatory progesterone levels (<2 nmol/l) were matched with ten cycles with normal preovulatory progesterone levels (>2 nmol/l). The sera of these four selected sets of treatments were stored for subsequent measurement of the concentrations of inhibin A, inhibin B, activin A and leptin. During ovarian hyperstimulation serum levels of inhibin A correlated significantly with those of progesterone (p < 0.001), whereas this correlation disappeared after the withdrawal of FSH administration. The rapid fall of progesterone levels during prolonged coasting contrasts with the continuing rise of estradiol concentration and indicates that the theca interna, not the granulosa, is the major source of preovulatory progesterone. Women failing to produce any increment of progesterone levels at the end of follicular development had significantly lower levels of inhibin A (p < 0.05), indicating that inhibin A may well be involved in mediating the signal of FSH from the granulosa to the theca interna.

Sympathetic pharmacological denervation in ageing rats: effects on ovulatory response and follicular population

The present study analyses the participation of ovarian innervation during reproductive senescence. We use the model of acute peripheral pharmacological sympathetic denervation with guanethidine in young (3 months old), middle-aged (12 months old) or old (18 months old) rats with spontaneous or induced ovulation. Ovarian levels of norepinephrine (NE) were measured by HPLC and the oestrous cycle, the number of ovulating animals and the percentage of atretic follicles were also assessed. Aged animals showed a progressive reduction in ovulatory capacity and an increase in ovarian NE content. Acute denervation increased the percentage of healthy follicles in 12- and 18-month-old rats compared with control adult animals. Combined treatment of denervation plus stimulation with gonadotrophins doubled the number of ova shed in young adult rats and restablished a partial ovulation in 12-month-old rats. The results suggest that ovarian noradrenergic innervation plays a modulator role in ovarian physiology during the ageing ovary process. The action of ovarian noradrenergic innervation seems to be associated with folliculogenesis and the ovarian response to gonadotrophins.

The celiac ganglion modulates LH-induced inhibition of androstenedione release in late pregnant rat ovaries

BackgroundAlthough the control of ovarian production of steroid hormones is mainly of endocrine nature, there is increasing evidence that the nervous system also influences ovarian steroidogenic output. The purpose of this work was to study whether the celiac ganglion modulates, via the superior ovarian nerve, the anti-steroidogenic effect of LH in the rat ovary. Using mid- and late-pregnant rats, we set up to study: 1) the influence of the noradrenergic stimulation of the celiac ganglion on the ovarian production of the luteotropic hormone androstenedione; 2) the modulatory effect of noradrenaline at the celiac ganglion on the anti-steroidogenic effect of LH in the ovary; and 3) the involvement of catecholaminergic neurotransmitters released in the ovary upon the combination of noradrenergic stimulation of the celiac ganglion and LH treatment of the ovary.MethodsThe ex vivo celiac ganglion-superior ovarian nerve-ovary integrated system was used. This model allows studying in vitro how direct neural connections from the celiac ganglion regulate ovarian steroidogenic output. The system was incubated in buffer solution with the ganglion and the ovary located in different compartments and linked by the superior ovarian nerve. Three experiments were designed with the addition of: 1) noradrenaline in the ganglion compartment; 2) LH in the ovarian compartment; and 3) noradrenaline and LH in the ganglion and ovarian compartments, respectively. Rats of 15, 19, 20 and 21 days of pregnancy were used, and, as an end point, the concentration of the luteotropic hormone androstenedione was measured in the ovarian compartment by RIA at various times of incubation. For some of the experimental paradigms the concentration of various catecholamines (dihydroxyphenylalanine, dopamine, noradrenaline and adrenaline) was also measured in the ovarian compartment by HPLC.ResultsThe most relevant result concerning the action of noradrenaline in the celiac ganglion was found on day 21 of pregnancy resulting in the inhibition of androstenedione release from the ovarian compartment. In addition on day 15 of pregnancy, LH placed in the ovarian compartment led to an inhibition of the release of androstenedione, and this inhibitory effect was further reinforced by the joint action of noradrenaline in the celiac ganglion and LH in the ovary. The levels of catecholamines in the ovarian compartment showed differences among the experiments; of significance, the joint treatment of noradrenaline in the celiac ganglion and LH in the ovary resulted in a remarkable increase in the ovarian levels of noradrenaline and adrenaline when compared to the effect achieved by either one of the compounds added alone.ConclusionOur results demonstrate that the noradrenergic stimulation of the celiac ganglion reinforces the LH-induced inhibition of androstenedione production by the ovary of late pregnant rats, and that this effect is associated with marked changes in the release of catecholamines in the ovary.

Taxonomic status of Ascocotyle (Phagicola) rara Arruda, Muniz-Pereira et Pinto, 2002 (Digenea: Heterophyidae)

Holotype and paratype of Ascocotyle (Phagicola) rara Arruda, Muniz-Pereira et Pinto, 2002, a heterophyid trematode recently described on the basis of two worms collected by Lauro Travassos in 1921 in the intestine of Ixobrychus exilis (Gmelin) from Brazil, were studied. The morphology of the worms revealed their conspecificity with Ascocotyle (Phagicola) angeloi Travassos, 1928 found in the same host. Both the taxa have a similar length (between 600 and 900 microm) and shape of the body (long pyriform), the long intestinal caeca reaching to the ovarian level, a long posterior muscular prolongation of the oral sucker and the prepharynx, transverse uterine loops situated between the ventral sucker and testes, and the gonotyl with more than 20 digitiform pockets. Consequently, A. (P.) rara is proposed as a junior synonym of Ascocotyle (Phagicola) angeloi.

Inhibitory effect of leptin on the rat ovary during the ovulatory process

The aims of this study were to investigate the negative action of leptin on some intraovarian ovulatory mediators during the ovulatory process and to assess whether leptin is able to alter the expression of its ovarian receptors. Immature rats primed with gonadotrophins were used to induce ovulation. Serum leptin concentration was diminished 4 h after human chorionic gonadotrophin (hCG) administration, whereas the ovarian expression of leptin receptors, measured by western blot, was increased by the gonadotrophin treatment. Serum progesterone level, ovulation rate and ovarian prostaglandin E (PGE) content were reduced in rats primed with equine chorionic gonadotrophin (eCG)/hCG and treated with acute doses of leptin (five doses of 5 mug each). These inhibitory effects were confirmed by in vitro studies, where the presence of leptin reduced the concentrations of progesterone, PGE and nitrites in the media of both ovarian explants and preovulatory follicle cultures. We also investigated whether these negative effects were mediated by changes in the expression of the ovarian leptin receptors. Since leptin treatment did not alter the expression of ovarian leptin receptor, the inhibitory effect of leptin on the ovulatory process may not be mediated by changes in the expression of its receptors at ovarian level, at least at the concentrations assayed. In summary, the ovulatory process was significantly inhibited in response to an acute treatment with leptin, and this effect may be due, at least in part, to the direct or indirect impairment of some ovarian factors, such as prostaglandins and nitric oxide.

Effect of Di(2-Ethylhexyl) Phthalate (DEHP) on Genital Organs from Juvenile Common Marmosets: I. Morphological and Biochemical Investigation in 65-Week Toxicity Study

Recent studies demonstrated that preadolescent male rats are more sensitive to testicular damage from exposure to DEHP than adults. Male and female marmosets were treated daily with 0, 100, 500, or 2500 mg/kg DEHP by oral gavage for 65 wk from weaning (3 mo of age) to sexual maturity (18 mo). No treatment-related changes were observed in male organ weights, and no microscopic changes were found in male gonads or secondary sex organs. Sperm head counts, zinc levels, glutathione levels, and testicular enzyme activities were comparable between groups. Electron microscopic examination revealed no treatment-related abnormalities in Leydig, Sertoli, or spermatogenic cells. Histochemical examination of the testis after 3β-hydroxysteroid dehydrogenase (3β-HSD) staining did not reveal any alterations in steroid synthesis in the Leydig cells. Thus, although marmoset monkeys were treated with 2500 mg/kg DEHP, throughout the pre- and periadolescent period, no histological changes were noted in the testes. For females, increased ovarian and uterine weights and elevated blood estradiol level were observed in higher dosage groups, 500 and 2500 mg/kg. These increased weights were associated with the presence of large corpus luteum, a common finding in older female marmosets. Although an effect on the female ovary cannot be completely ruled out, no abnormal histological changes were observed in the ovaries or uteri in comparison to controls. No increases in hepatic peroxisomal enzyme activities were noted in treated groups; isolated hepatic enzyme activities (P-450 contents, testosterone 6β-hydroxylase, and lauric acid ω-1ω-hydroxylase activities) were increased in males and/or females of either the mid- or high-dose groups, but no consistent dose-related trend was observed.

Internal dose-effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in gonadotropin-primed weanling rat model

Single sc injection of 5 IU equine chorionic gonadotropin (eCG) induces ovulation in weanling female rats 3 days later. It has been shown that treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) 24 h before eCG injection reduces eCG-stimulated ovarian hypertrophy and inhibits ovulation. The present study intended to compare internal dose-effects of TCDD between these endpoints and representative endpoints for TCDD toxicity, such as weights of the liver and thymus, in weanling female rats given orally 0, 1, 4 or 16 microg/kg TCDD 24 h before eCG injection on postnatal day 25. Measurement of plasma TCDD concentrations by ELISA at 6, 72 and 96 h after TCDD revealed that significant levels of TCDD were maintained in systemic circulation until 96 h (on the day of induced ovulation) with the highest level at 6 h after TCDD treatment. Ovarian TCDD concentrations varied similarly and tended to be higher than those in the thymus at all time points, whereas hepatic concentrations of TCDD were the highest among the tissues. Although > or = 4 microg/kg TCDD affected the weights of the thymus and liver, no differences were observed in ovarian weights at any time point or in ovulation between corn oil-treated and TCDD-treated groups. Furthermore, ovarian levels of representative mRNAs in follicles were not affected by TCDD treatment. Since TCDD increased the amount of cytochrome P450 1A1 mRNA in the ovary, the administered TCDD stimulated the aryl hydrocarbon receptor-signaling pathway. From these results, we concluded that thymus weights of weanling female rats responded to TCDD at a lower internal dose as compared with that ovarian hypertrophy and follicular growth from early antral stage to ovulation would respond to.

Altered expression of Fas/Fas ligand/caspase 8 and membrane type 1-matrix metalloproteinase in atretic follicles within dehydroepiandrosterone-induced polycystic ovaries in rats

One of the characteristics of polycystic ovary syndrome (PCOS) is the presence of cystic follicles in various stages of growth and atresia, the latter of which is known to be the result of apoptosis and tissue remodeling. To further investigate the process of follicular atresia, we compared ovarian expression and localization of Fas, Fas ligand (FasL), casapse-8 and membrane-type1 matrix metalloproteinase (MT1-MMP) in rats treated with dehydroepiandrosterone (DHEA) as a model of PCOS, and in control rats. We found that the numbers of TdT-mediated dUTP-biotin nick end-labeling (TUNEL)-positive follicles were significantly higher in ovaries from PCOS rats than in those from control rats (P < 0.05), as were ovarian levels of FasL mRNA and protein, processed caspase-8 protein and MT1-MMP mRNA. Correspondingly, we also observed an increase in the level of MTI-MMP catalytic activity and a decrease in the level of pro-caspase-8 protein. In addition, immunohistochemical analyses showed that MT1-MMP and FasL co-localize with TUNEL-positive apoptotic granulosa cells within atretic follicles of PCOS ovaries. Our results suggest that under the PCOS-like conditions induced by DHEA, the Fas/FasL/Caspase-8 (death receptor dependent) pathway is pivotal for follicular atresia, and that increased levels of MT1-MMP likely play an important role in tissue remodeling during structural luteolysis.

Polycystic ovary syndrome: etiology and pathogenesis

To provide a review of the pathogenesis of polycystic ovary syndrome. Literature survey. Three major pathophysiologic hypotheses have been proposed to explain the clinical findings of polycystic ovary syndrome (PCOS) related to three major laboratory findings: the LH hypothesis, the insulin hypothesis and the ovarian hypothesis. Although the presence of many small follicles with a high androgen to estrogen ratio was first thought to represent a high rate of follicular atresia in polycystic ovaries, recent studies have demonstrated that the granulosa cells are viable and able to respond to FSH stimulation with normal increases in estradiol production. Thus, a new hypothesis has arisen that FSH activity is somehow blocked at the ovarian level. PCOS is a syndrome involving defects in primary cellular control mechanisms that result in the expression of chronic anovulation and hyperandrogenism. In this syndrome, the relation between the various parameters is of particular interest. These relations constitute the cornerstone of the pathogenesis of PCOS. The fact that the pathogenesis of PCOS has not yet been clarified, despite the plethora of relative information, may be the result of a general way of thinking in the interpretation of several scientific data, and especially those that refer to biochemical phenomena. The use of the various models of the theory of chaos, that permits a concrete approach for the interpretation of data, may constitute an optional procedure for the future understanding of the association of different parameters and their disturbances in the pathogenesis of the polycystic ovary syndrome.

Aetiology and pathogenesis of cystic ovarian follicles in dairy cattle: a review

Cystic ovarian follicles (COF) are an important ovarian dysfunction and a major cause of reproductive failure in dairy cattle. Due to the complexity of the disorder and the heterogeneity of the clinical signs, a clear definition is lacking. A follicle becomes cystic when it fails to ovulate and persists on the ovary. Despite an abundance of literature on the subject, the exact pathogenesis of COF is unclear. It is generally accepted that disruption of the hypothalamo-pituitary-gonadal axis, by endogenous and/or exogenous factors, causes cyst formation. Secretion of GnRH/LH from the hypothalamus-pituitary is aberrant, which is attributed to insensitivity of the hypothalamus-pituitary to the positive feedback effect of oestrogens. In addition, several factors can influence GnRH/LH release at the hypothalamo-pituitary level. At the ovarian level, cellular and molecular changes in the growing follicle may contribute to anovulation and cyst formation, but studying follicular changes prior to cyst formation remains extremely difficult. Differences in receptor expression between COF and dominant follicles may be an indication of the pathways involved in cyst formation. The genotypic and phenotypic link of COF with milk yield may be attributed to negative energy balance and the associated metabolic and hormonal adaptations. Altered metabolite and hormone concentrations may influence follicle growth and cyst development, both at the level of the hypothalamus-pituitary and the ovarian level.

A case report of Pseudo-Meigs' syndrome associated with ovarian serous cystadenocarcinoma

Pseudo-Meigs' syndrome is a rare condition that includes hydrothorax and/or ascites secondary to ovarian neoplasms other than benign primary tumors. A 67-year-old woman presented with ascites, hydrothorax, left ovarian mass and elevated CA-125 level. The mass was removed and revealed serous cystadenocarcinoma. The immediate and complete resolution of symptoms and rapid decline of CA-125 level to normal value was achieved post-operatively. One month after surgery, she had no evidence of ascites or pleural effusion. We report Pseudo-Meigs' syndrome associated with ovarian serous cystadenocarcinoma and elevated CA-125 level.

Thiazolidinediones and Fertility in Polycystic Ovary Syndrome (PCOS)

Polycystic ovary syndrome (PCOS) is the most frequent cause of female infertility. The treatment of PCOS patients with insulin sensitizers, such as metformin or thiazolidinediones, increases the ovulation rate and the number of successful pregnancies. The positive action of the insulin-sensitizing treatments could be explained by a decrease in the peripheral insulin resistance but also by a direct action at the ovarian level. We report in this review different hypotheses of thiazolidinediones actions to improve PCOS (steroid secretion by ovarian cells ; insulin sensitivity in muscle and adipocyte and fat redistribution).

Does gravidity influence the success of in vitro fertilization–embryo transfer cycles?

Objective. To evaluate the influence of gravidity on the results of in vitro fertilization (IVF)–embryo transfer (ET) cycles.Patients and methods. All consecutive women aged <35 years admitted to our IVF unit from January 2002 to December 2004 were enrolled in the study. Only patients undergoing one of their first three IVF cycle attempts were included. Gravidity, ovarian stimulation characteristics, number of oocytes retrieved, number of embryo transferred and clinical pregnancy rate were assessed.Results. Three hundred and forty-two consecutive IVF cycles were evaluated. One hundred and sixty-one cycles were from nulligravidas and 181 from women with a history of at least one previous clinical pregnancy. Forty-eight (29.8%) clinical pregnancies were observed in the nulligravida group and 56 (30.9%) in the gravida group. There were no differences between nulligravidas and gravidas in causes of infertility, length of ovarian stimulation, peak estradiol and progesterone levels, number of oocytes retrieved, fertilization rate and number of embryos transferred. Gravidas were significantly older (30.4 vs. 27.6 years, p < 0.001) and used more gonadotropin ampoules (36.1 vs. 31.8, p < 0.004) compared with the nulligravidas.Conclusions. Patient gravidity has no influence on the likelihood of achieving pregnancy in IVF–ET cycles.

Does injection of prostaglandin F 2α (PGF 2α) cause ovulation in anestrous Western White Face ewes?

In a previous study in our laboratory, treatment of non-prolific Western White Face (WWF) ewes with PGF 2α and intravaginal sponges containing medroxyprogesterone acetate (MAP) on ∼Day 8 of a cycle (Day 0 = first ovulation of the interovulatory interval) resulted in ovulations during the subsequent 6 days when MAP sponges were in place. Two experiments were performed on WWF ewes during anestrus to allow us to independently examine if such ovulations were due to the direct effects of PGF 2α on the ovary or to the effects of a rapid decrease in serum concentrations of progesterone at PGF 2α-induced luteolysis. Experiment 1: ewes fitted with MAP sponges for 6 days ( n = 12) were injected with PGF 2α ( n = 6; 15 mg im), or saline ( n = 6) on the day of sponge insertion. Experiment 2: ewes received progesterone-releasing subcutaneous implants ( n = 6) or empty implants ( n = 5) for 5 days. Six hours prior to implant removal, all ewes received a MAP sponge, which remained in place for 6 days. Ewes from both experiments underwent ovarian ultrasonography and blood sampling once daily for 6 days before and twice daily for 6 days after sponge insertion. Additional blood samples were collected every 4 h during sponge treatment. Experiment 1: 4–6 (67%) PGF 2α-treated ewes ovulated ∼1.5 days after PGF 2α injection; these ovulations were not preceded by estrus or a preovulatory surge release of LH, and resulted in transient corpora hemorrhagica (CH). The growth phase was longer ( P < 0.05) and the growth rate slower ( P < 0.05) in ovulating versus non-ovulating follicles in PGF 2α-treated ewes. Experiment 2: in ewes given progesterone implants, serum progesterone concentrations reached a peak (1.72 ng/mL; P < 0.001) on the day of implant removal and decreased to basal concentrations (<0.17 ng/mL; P < 0.001) within 24 h of implant removal. No ovulations occurred in either the treated or the control ewes. We concluded that ovulations occurring after PGF 2α injection, in the presence of a MAP sponge, could be due to a direct effect of PGF 2α at the ovarian level, rather than a sudden decline in circulating progesterone concentrations.

Comparison of Granulosa Cell Aromatase Activity Between Poor and Good Responders Undergoing IVF

The etiology of poor responders is not well understood. We have previously shown that aromatase activity (AA) is correlated with pregnancy potential. It is proposed that poor responders may have insufficient AA at the ovarian level therefore limiting estrogen production in follicles. The aims of this study were to investigate the relationship between the AA of granulosa cells (GCs) in poor and good responders to provide a better understanding of the ovarian hormonal milieu and stimulation dynamics of these patients.