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PubMed2005

Ovarian follicular development and oocyte quality in anestrous ewes treated with melatonin, a controlled internal drug release (CIDR) device and follicle stimulating hormone.

The objective of the current study was to determine the effects of hormonal treatments on ovarian follicular development and oocyte quality in anestrous ewes. Multiparous crossbred (RambouilletxTarghee) ewes were given melatonin implants (MEL) and/or controlled internal drug release (CIDR) devices in conjunction with follicle stimulating hormone (FSH) during anestrus (March-May). In Experiment 1, ewes (n=25) were assigned randomly to four groups (n=4-7/group) in a 2x2 factorial arrangement [+/-MEL and +/-CIDR], resulting in Control (no treatment), CIDR, MEL, and MEL/CIDR groups, respectively. Ewes received an implant containing 18 mg of melatonin (Melovine) on Day 42 and/or a CIDR from Days 7 to 2 (Day 0: oocyte collection). In Experiment 2, ewes (n=12) were assigned randomly to two groups (n=6/group; 1CIDR or 2CIDR) and received the same type of melatonin implant on Day 60. All ewes received a CIDR device from Days -22 to -17 and 2CIDR ewes received an additional CIDR device from Days -10 to -2. In both experiments, ewes were given FSH im twice daily (morning and evening) on Days -2 and -1 (Day -2: 5 units/injection; Day -1: 4 units/injection). On the morning of Day 0, ovaries were removed, follicles>or=1 mm were counted, and oocytes were collected. Thereafter oocytes were matured and fertilized in vitro. In Experiment 1, the number of visible follicles and the rates of oocyte recovery and in vitro maturation were similar (P>0.10) for Control, CIDR, MEL and MEL/CIDR (overall 29.7+/-2.9%, 89.9+/-7.1% and 95.0+/-2.0%, respectively). The rates of in vitro fertilization (IVF) were lower (P<0.01) for CIDR and MEL/CIDR than for Control and MEL groups (10.3% and 10.1% versus 20.0% and 18.5%, respectively). In Experiment 2, the number of visible follicles, and the rates of oocyte recovery and in vitro maturation were similar (P>0.10) for 1CIDR and 2CIDR groups (overall 27.3+/-3.2%, 92.1+/-2.7% and 90.2+/-1.9%, respectively). However, the rates of IVF were lower (P<0.01) for 2CIDR than 1CIDR group (30.2% versus 58.0%, respectively). In summary, when treatment with P4 commenced only 2 d before oocyte collection, rates of IVF were reduced in both experiments. Therefore, progestin treatment protocols used in ovine IVF programs should be carefully designed to minimize adverse effects on fertilization rates. In addition, melatonin treatment did not affect follicular development and oocyte quality for anestrous ewes.

Anestrus↗
PubMed1995

Hormonal serum profiles and follicular development after intramuscular and pulsatile intravenous administration of human menopausal gonadotrophin.

A study was performed to compare, in a randomized way, the effect of pulsatile intravenous (i.v.) and intramuscular (im) human menopausal gonadotrophin (hMG) administration on hormonal serum profiles and follicular development in in vitro fertilization (IVF). Fourteen IVF patients participated in the study, aged between 20 and 40 years, with a normal endocrine profile, no hormonal medication used for at least 3 months previously, no endometriosis, both ovaries present and a normal male factor. Seven patients were treated with im hMG at a daily dose of 150 IU and seven patients with pulsatile i.v. hMG at a daily dose of 112.5 IU, in both cases in combination with buserelin. Ultrasonography was performed every other day during the stimulation phase and blood samples were collected once daily up to five times a day during the entire IVF cycle. Serum concentrations of follicle-stimulating hormone, luteinizing hormone, 17 beta-oestradiol, progesterone and human chorionic gonadotrophin were determined. There were no differences in hormonal profiles between the two groups. The numbers of retrieved oocytes, fertilization rates and mean embryo quality were identical in this study, as was follicular growth. In conclusion, in the present randomized study no differences were observed in hormonal levels or follicular development after im and pulsatile i.v. hMG treatment.

Adult↗
PubMed1999

Effect of stress-like concentrations of cortisol on follicular development and the preovulatory surge of LH in sheep.

Stress-like concentrations of cortisol increase the negative feedback potency of oestradiol in castrated male sheep. A similar cortisol-dependent response in female sheep might be expected to suppress gonadotrophin secretion and impair follicular development and ovulation. The oestrous activity of 21 female sheep was synchronized using progestogen-treated vaginal pessaries to test this hypothesis. Stress-like concentrations of cortisol (60-70 ng ml-1) were established by continuous infusion of cortisol (80 micrograms kg-1 h-1; n = 13) beginning 5 days before, and continuing for 5 days after, pessary removal. Control animals (n = 8) received a comparable volume of vehicle (50% ethanol-saline) over the 10 day infusion period. Serum concentrations of oestradiol increased progressively in control sheep during the 48 h immediately after pessary removal. This increase in serum oestradiol was blocked or significantly attenuated in sheep receiving stress-like concentrations of cortisol. Preovulatory surge-like secretion of LH was apparent in control animals 58.5 +/- 2.1 h after pessary removal. In contrast, surge-like secretion of LH was not observed during the 5 days after pessary removal in 54% (7 of 13) of sheep receiving cortisol. Moreover, the onset of the surge was significantly delayed in the cortisol-treated ewes that showed surge-like secretion of LH during the infusion period. The ability of episodic pulses of exogenous GnRH to override the anti-gonadal effect of cortisol was examined in a second study. Oestrous activity of 12 ewes was synchronized using progestogen-containing pessaries as described above. Ewes were randomly assigned to one of three treatment groups (n = 4 ewes per group). Animals received cortisol (100 micrograms kg-1 h-1; groups 1 and 2) or a comparable volume of vehicle (group 3) beginning 5 days before, and continuing for 2 days after, pessary removal. Pulses of GnRH (4 ng kg-1 h-1, i.v.; group 1) or saline (groups 2 and 3) at 1 h intervals were initiated at pessary removal and continued for 48 h. Serum concentrations of oestradiol were not significantly increased after pessary removal in sheep receiving cortisol alone. Conversely, serum concentrations of oestradiol increased progressively during the 48 h after pessary removal in control ewes and in ewes receiving cortisol and GnRH. At the end of infusion, serum concentrations of oestradiol did not differ (P > 0.05) between control (7.7 +/- 0.8 pg ml-1) ewes and ewes receiving cortisol and episodic GnRH (6.4 +/- 1.3 pg ml-1). Moreover, these values were significantly greater (P < 0.05) than the serum concentrations of oestradiol in animals receiving cortisol (1.0 +/- 0.4 pg ml-1) alone. Collectively, these data indicate stress-like concentrations of cortisol block or delay follicular development and the preovulatory surge of LH in sheep. In addition, episodic GnRH overrides cortisol-induced delay in follicular maturation.

Analysis of Variance↗
PubMed2000

Dexamethasone or triamcinolone increases follicular development in immature female rats.

We have previously reported that dexamethasone increased follicle-stimulating hormone (FSH) secretion via suppression of inhibin in immature female rats. In the present study, we investigated the effects of dexamethasone or triamcinolone on follicular development and ovarian functions (estradiol and inhibin secretion) in equine chorionic gonadotropin (eCG)-primed immature female rats. Dexamethasone significantly increased the number of ovulated oocytes in immature female rats treated with 5 i.u. eCG. Serum concentration of FSH in eCG-treated female rats was increased by administration of dexamethasone or triamcinolone, showing the peak value at 9 h after its administration, although the levels of inhibin markedly decreased at that time. Serum concentrations of inhibin and estradiol in eCG-treated female rats increased at 24 h after administration of dexamethasone or triamcinolone. These results demonstrate that dexamethasone or triamcinolone increases FSH secretion, and the excess amount of FSH strongly stimulates follicular development cooperating with exogenous eCG.

Animals↗
PubMed1993

Ultrasonographic monitoring of follicular development, ovulation and the early luteal phase in the bitch.

Follicular development, ovulation and the early luteal phase in 15 oestrous cycles of 13 individual bitches were monitored daily by ultrasonography using a 7.5 MHz sector scanner transducer. These findings were compared with vaginal cytology and changes in the peripheral plasma concentrations of oestradiol, luteinizing hormone (LH) and progesterone. Both ovaries were imaged throughout the period of study. Follicles were identified as anechoic spherical structures as early as day 1 of pro-oestrus in two cases and on days 3-4 in 13 cases. The average follicular size increased from 3.7 +/- 0.6 mm to 6.9 +/- 0.7 mm (P < 0.001) between day -5 and the LH surge (day 0). The anechoic structures then increased in size to 7.5 +/- 0.7 mm (P < 0.05) until day 2 after the LH surge; their diameters continued to increase during corpus luteum development, up to 8.1 +/- 0.6 mm (P < 0.001) on the first day of dioestrus. The average number of follicles counted imaged on the day of the LH surge was 3.3 +/- 0.4 on the left ovary and 3.7 +/- 0.7 on the right ovary. The rapid disappearance of the anechoic antrum, corresponding to ovulation, was detected in only two bitches. In the remaining cases follicular rupture was not detected; however, starting at the LH surge, a gradual thickening of the antral wall occurred. This corresponded to a progressive obliteration of the anechoic region and was characteristic of the postovulatory corpora lutea. These changes led to a significant decrease (P < 0.05) in the number of anechoic structures to 2.4 +/- 0.5 on the left ovary and 3.3 +/- 0.5 on the right ovary by day 1 of dioestrus. During the follicular phase, the mean increase in oestradiol concentration was correlated with follicular size (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Correlation between LH response to challenges with GNRH and naloxone during lactation, and LH secretion and follicular development after weaning in the sows.

The aim of this study was of establishing a correlation between endogenous LH secretion and the magnitude of the LH response to challenges with GnRH and the opioid antagonist naloxone during lactation, and between these characteristics and LH secretion and follicular development after weaning. Sows (n = 9) were sampled for 6 h at day 2 post-partum, for 12 h on day 26 of lactation and for 6 h immediately after weaning at day 27 of lactation. Four hours after the beginning of sampling at day 26 of lactation all sows were injected with 2 mg/kg i.v. of naloxone hydrochloride and 5 h later with 100 microg/sow of GnRH. Follicular development was studied in all sows at slaughter the day after weaning. There was an effect of time (sampling period; P < 0.001) on mean plasma LH, with an increase (P < 0.05) in LH the day after weaning compared to mean LH concentrations during lactation. Naloxone and GnRH treatment both increased (P < 0.05) mean LH concentrations. A positive relationship (r = 0.58, P < 0.01) between mean plasma LH after GnRH and after weaning was established. Although there were differences (P < 0.001) between sows in follicular fluid volume, there were no correlations between mean follicular fluid volume and mean LH concentrations after GnRH or after weaning. These data indicate that the LH response to GnRH during late lactation could be useful predictor of LH activity after weaning. However, none of the measures of endogenous or induced LH secretion were associated with differences in ovarian follicular size after weaning. Direct evidence is therefore still needed for a functional link between differences in LH in lactation and differences in fertility after weaning.

Animals↗
PubMed1994

Circulating nitrite/nitrate levels increase with follicular development: indirect evidence for estradiol mediated NO release.

Ovarian dysfunction as well as impaired release of endothelium-derived nitric oxide (NO) is associated with increased incidence of cardiovascular disease in postmenopausal women. Estrogen replacement therapy in postmenopausal women has a cardioprotective effect. Hence, using follicular development (FD) phase of the menstrual cycle of normal women (n = 7) and of patients undergoing in vitro fertilization (n = 16), we tested whether ovarian/sex hormones modulate NO-release. Levels of nitrite/nitrate (stable metabolites of NO), 17 beta-estradiol (E), progesterone (P), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured in serum collected during FD-phase. Serum nitrite/nitrate levels increased (p < .01) with the normal, as well as hormonally-induced FD and correlated with increases in serum E levels (r2 = 0.67; p < .01), but not with P, FSH and LH (p > .05). Post-ovulatory increase in P and LH levels decreased serum nitrite/nitrate levels (p < .05), even in presence of high E levels. In conclusion, nitrite/nitrate increase with follicular development, an effect that is potentially mediated by E induced NO release.

Adult↗
PubMed1986

Ultrasonic and endocrinologic investigation of ovarian follicle and free fluid in cul-de-sac for monitoring follicular development and ovulation.

The accuracy of ultrasound as a means of monitoring follicular development and ovulation detection was studied in 31 infertile women. The follicular diameter measured by ultrasound correlated well actual diameter found during laparotomy (r = 0.88), and estradiol-17 beta (E2) and progesterone in follicular fluid aspirated from large follicles (greater than or equal to 16 mm) indicated high levels. Furthermore, in 23 out of the 55 cycles, ultrasound examinations demonstrated free fluid in cul-de-sac at ovulation, and concentrations of E2 and progesterone (P) in peritoneal fluid by the puncture of cul-de-sac dramatically increased after ovulation. We suggested that ultrasound monitoring provided a reliable measure of follicular growth and prediction of ovulation, and a combined use of ultrasound and puncture of cul-de-sac could be developed into a new tool for the study of the mechanism of human ovulation.

Adult↗
PubMed2006

Localization of cystathionine beta synthase in mice ovaries and its expression profile during follicular development.

BACKGROUND: In vitro fertilization (IVF) researches have suggested that cystathionine beta synthase (CBS) is involved in oocyte development. However, little is known about the regional and cellular expression patterns of CBS in the ovary. The purpose of this study was to analyze the localization of CBS in mice ovaries and to investigate the expression profile during follicular development. METHODS: We used in situ hybridization and immunohistochemical analysis to determine CBS expression in the ovaries of female Balb/c mice. Then the follicles were collected from F1 (C57BL x Balb/c) mice and cultured in vitro. With the method of semi-quantitative RT-PCR, we also investigated the expression profile of CBS during follicular development. RESULTS: CBS was absent in the oocytes, although it was ubiquitously expressed in the ovary with the strongest expression in follicular cells at all stages. In late antral follicles, CBS expression was markedly higher in granulosa cells located close to the antrum and in cumulus cells around the oocyte. The semi-quantitative RT-PCR showed that CBS mRNA was detected in follicles at all stages in vitro. In cumulus-oocyte complexes superovulated, CBS expression also increased rapidly. CONCLUSIONS: CBS was located mainly in the follicular cells in the ovaries. The level of CBS expression is high in follicles during folliculogenesis in mice. Differences in the CBS expression profile between oocyte and follicular cells suggest a role for CBS as a mediator in interactions between oocyte and granulosa cells.

Animals↗
PubMed2003

VavP-Bcl2 transgenic mice develop follicular lymphoma preceded by germinal center hyperplasia.

In human follicular lymphoma the t(14; 18) chromosome translocation activates the antiapoptotic oncogene Bcl2 by linking it to the immunoglobulin heavy chain (IGH) locus. Transgenic mice expressing Bcl2 controlled by an Igh enhancer (E mu) do not develop follicular lymphoma, although they do have an increased incidence of other B-lymphoid neoplasms. We have now analyzed tumorigenesis in mice bearing a Bcl2 transgene controlled by Vav gene regulatory sequences (VavP), which confer expression in multiple hematopoietic lineages. Unlike E mu-Bcl2 mice, many VavP-Bcl2 mice older than 10 months developed follicular lymphoma. Young VavP-Bcl2 mice had an overabundance of enlarged germinal centers and greatly elevated numbers of cycling B cells that had undergone IgH class switching and V-gene hypermutation. The peripheral T-cell compartment was larger in the VavP-Bcl2 mice than in E mu-Bcl2 strains and, notably, CD4 T cells were 5-fold increased over normal. The germinal center hyperplasia required CD4 T cells, because it could be abolished by anti-CD4 antibody in vivo. VavP-Bcl2 mice also had a propensity to develop kidney disease of the autoimmune type. We suggest that the increased survival capacity of B and T cells fosters prolonged germinal center reactions, and that autoreactivity and hypermutation conspire to generate follicular lymphoma.

Animals↗
PubMed1994

Recombinant human follicle-stimulating hormone stimulates multiple follicular growth, but minimal estrogen production in gonadotropin-releasing hormone antagonist-treated monkeys: examining the role of luteinizing hormone in follicular development and steroidogenesis.

The two-cell theory predicts that follicular steroidogenesis requires the coordinate actions of both FSH and LH; however, the role of LH in follicular growth is less clear. The present study was designed to investigate the relative importance of LH and FSH in follicular growth and steroidogenesis. Cynomolgus monkeys were treated with a GnRH antagonist (antide; 3 mg/kg.day) for 20 days beginning in the midluteal phase of the menstrual cycle. After 10 days of antide administration, monkeys were injected with recombinant human FSH (rhFSH; 10 IU; n = 3), human menopausal gonadotropin (hMG; 10 IU; n = 3), or FSH plus 0.5 IU LH (n = 3) twice daily for 10 days. rhFSH stimulated multiple follicular development; however, peak serum estradiol levels were only 943 +/- 195 pmol/L. In contrast, monkeys treated with the same dose of hMG had significantly higher (P < 0.05) peak estradiol levels (6013 +/- 1322 pmol/L). The addition of 0.5 IU LH to the rhFSH treatment resulted in serum estradiol levels similar to those in monkeys treated with rhFSH only. Importantly, no differences in follicle number or size were evident among these treatment groups. Follicular fluid estradiol levels were consistent with serum levels (rhFSH, 187 +/- 11 nmol/L; hMG, 1531 +/- 173 nmol/L). Even larger proportional differences in follicular fluid androstenedione (rhFSH 13.6 +/- 1.4 nmol/L; hMG, 307 +/- 97.7 nmol/L) levels were found. The results in this LH-deficient primate model suggest that FSH alone is capable of stimulating ovarian follicular growth; however, the resulting follicles manifest minimal estradiol production, probably due to deficiencies in the LH-induced precursors to estradiol.

Androstenedione↗
PubMed1994

Expression of 17 beta-hydroxysteroid dehydrogenase in the rat ovary during follicular development and luteinization induced with pregnant mare serum gonadotrophin and human chorionic gonadotrophin.

Antibodies against human placental 17 beta-hydroxysteroid dehydrogenase (17-HSD) and 17-HSD cDNA were used to study the expression of the corresponding enzyme in the immature rat ovary during follicular development and luteinization, which were induced by treating the animals with pregnant mare serum gonadotrophin (PMSG) or with PMSG followed by human chorionic gonadotrophin (hCG). Immuno-blot analysis indicated that the M(r) of the 17-HSD expressed in rat granulosa cells was 35,000, as previously shown for the human placental enzyme. In immunohistochemical studies of untreated immature rat ovaries, only the granulosa cells from small antral follicles were stained. One day after PMSG treatment, strong expression of 17-HSD was observed in the granulosa cells of growing Graafian follicles. A marked decrease in enzyme expression was observed in preovulatory follicles on day 2 of PMSG treatment, starting from the basal layers of granulosa cells and progressing toward the luminal cells. No 17-HSD expression was detected in luteinized follicles or corpora lutea 22 h after hCG injection. The stroma and theca cells were negative for 17-HSD staining. In Northern hybridization analyses, two 17-HSD mRNAs were detected (1.4 and 1.7 kb). The strongest expression for both mRNAs was detected after 1 day of PMSG treatment, coinciding with maximal immunostaining of the enzyme protein. Down-regulation of 17-HSD observed by immunohistochemistry was reflected in a similar decrease in mRNA expression and the signals were almost undetectable 22 h after hCG injection. Our data suggest that 17-HSD expression in rat granulosa cells is up-regulated during follicular development and, thereafter, the enzyme expression is down-regulated during luteinization.

17-Hydroxysteroid Dehydrogenases↗
PubMed2003

Relationship between FoxO1 protein levels and follicular development, atresia, and luteinization in the rat ovary.

FoxO1 is a transcription factor implicated in a growing number of physiological processes, including apoptosis, cell cycle progression, and insulin signaling. Recent findings indicate that FSH and growth factors influence ovarian functions in part through regulation of FoxO1. The present study utilized immunohistochemical analysis to determine the ovarian localization and regulation of FoxO1 protein levels in neonatal rats, immature rats during gonadotropin-induced follicular development, ovulation, and luteinization, and in spontaneously developing ovarian cysts of aging rats. In postnatal rats, FoxO1 immunoreactivity was very faint in ovaries of 5- and 10-day-old females. In contrast, strong immunoreactivity was observed in granulosa cells of larger developing follicles at 25 days of age. To stimulate follicle development, immature female rats received equine chorionic gonadotropin (eCG) followed 52 h later by an ovulatory dose of human chorionic gonadotropin (hCG). Prior to gonadotropin treatment, moderate FoxO1 immunoreactivity was observed in granulosa cells of small follicles. Subsequently, treatment with eCG markedly decreased FoxO1 protein levels in granulosa cells of healthy antral and preovulatory follicles. Interestingly, FoxO1 staining was observed in cumulus and antral, but not mural granulosa cells of preovulatory follicles. Induction of ovulation and luteinization with hCG further decreased ovarian FoxO1 levels, with no staining evident in corpora lutea. At all time points, the most intensive FoxO1 staining was observed in granulosa cells of atretic follicles, with predominantly nuclear localization. Similarly, while FoxO1 levels were low in granulosa cells of preovulatory follicles in proestrous rats, FoxO1 staining was intense in granulosa cells of spontaneously developing cystic follicles in aged, acyclic females. Together, these findings indicate that FoxO1 is expressed in a regulated, cell-specific manner during ovarian follicular development, atresia and luteinization, suggesting roles in these physiological processes.

Aging↗
PubMed1998

Mouse oocytes regulate granulosa cell steroidogenesis throughout follicular development.

Mouse oocytes secrete a factor(s) that inhibits progesterone and enhances estradiol production by granulosa cells. This study determined the ability of mouse oocytes to secrete this steroid-regulating factor during oocyte growth and the ability of granulosa cells to respond to the factor during follicular development. Oocyte-granulosa cell complexes from preantral and antral follicles were oocytectomized (OOX; oocytes microsurgically removed) and cultured for up to 48 h with FSH (150 ng/ml) and testosterone (500 nM). At all stages of development examined, OOX complexes produced more progesterone than did intact complexes, from 1.45-fold for early growing follicles to 23-fold for complexes from antral follicles. Significant estradiol production was restricted to intact complexes from late antral follicles. Progesterone accumulation by OOX complexes cocultured with oocytes was inhibited by all stages of oocytes examined, with maximal inhibition by fully grown oocytes. Ovulated complexes produced large quantities of progesterone, even though oocytes secreted progesterone-inhibitory factor, because of a desensitization of cumulus cells to the factor during their terminal differentiation. Even in the presence of abundant pregnenolone, OOX complexes showed reduced ability to produce and/or accumulate progesterone in the presence of oocytes, suggesting that the oocyte-secreted factor, either directly or indirectly, regulates the activity of 3beta-hydroxysteroid dehydrogenase and/or progesterone metabolism. These results demonstrate that oocytes secrete a factor with steroid-regulating activity in increasing amounts and/or potency during follicular development, but responsiveness of cumulus cells to this factor declines during luteinization.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Improvement of follicular development rather than gonadotrophin secretion by thyroxine treatment in infertile immature hypothyroid rdw rats.

Despite extensive study of reproductive abnormalities in female hypothyroid animals, little is known of folliculogenesis and gonadotrophin secretion in spontaneously hypothyroid animals, especially in response to exogenous hormone treatment. In this study, follicular development and plasma hormone concentrations in the presence or absence of thyroxine and eCG treatment were investigated in infertile immature spontaneously hypothyroid rdw rats. Administration of thyroxine once a day from day 21 to day 29 after birth resulted in increases in body weight (P < 0.001) and ovary mass on day 30 (P < 0.01). Similar populations of both healthy and atretic antral follicles ranging from 101 to 400 micrometer in diameter were observed in control rdw and normal rats. In rdw rats, thyroxine treatment markedly increased the number of healthy antral uniovular follicles 101-400 or > 550 micrometer in diameter in the absence or presence of eCG, respectively. Combined treatment of thyroxine and eCG in rdw rats also markedly increased the number of healthy antral biovular follicles. Thyroxine treatment did not affect the population of atretic antral follicles, but resulted in decrease in the number of atretic large antral follicles (> 400 microm) in the presence of eCG. Plasma oestradiol concentrations in rdw rats given both thyroxine and eCG were significantly higher than they were in rdw rats given eCG alone (P < 0.001). There were no significant differences in plasma FSH concentrations on day 28 between rdw (10.7 +/- 1.6 ng ml(-1)) and normal rats (12.0 +/- 1.4 ng ml(-1); P > 0. 05). Although there were no significant differences in plasma LH concentrations between control rdw (1.9 +/- 0.1 ng ml(-1)) and normal rats on day 30 (1.8 +/- 0.1 ng ml(-1); P > 0.05), eCG treatment increased plasma LH to a peak concentration 52 h after injection in normal (24.9 +/- 2.4 ng ml(-1)) but not in rdw rats treated with thyroxine (4.8 +/- 0.3 ng ml(-1); P < 0.05). In conclusion, the results of the present study indicate that thyroxine treatment improves follicular development but does not rescue the defect of the preovulatory surge of LH in eCG-primed rdw rats.

Animals↗
PubMed1988

Follicular development is impaired by inhibitors of serine proteases in the rat.

Serine proteases such as plasminogen activators are produced by granulosa cells both in vivo and in vitro and have been implicated in the process of ovulation. For a study of potential roles of serine proteases in early follicular development, immature rats were injected with pregnant mare serum gonadotropin, followed 2 hours later by laparotomy and injection of the serine protease inhibitors benzamidine and epsilon-aminocaproic acid into the bursa of one ovary. As a control, saline solution was injected into the contralateral bursa. Animals were put to death 48 hours after injection of serine protease inhibitors, and three to five randomly selected longitudinal sections were evaluated by computerized morphometry. The area occupied by antral follicles relative to the total cross-sectional area of each section was computed. Resultant ratios from serine protease inhibitor-treated ovaries were compared with those from contralateral control ovaries. Ninety-three percent of serine protease inhibitor-treated ovaries showed a reduction in antral follicular size when compared with corresponding control ovaries, which is indicative of inhibitory effects of serine protease inhibitor treatment on folliculogenesis. To further investigate this effect, ovulation was induced by human chorionic gonadotropin administration 48 hours after pregnant mare serum gonadotropin and 46 hours after serine protease inhibitor or saline solution treatment. Animals were put to death 20 hours later and the number of oocytes ovulated into oviducts was determined. Oviducts from serine protease inhibitor-treated ovaries contained 51% fewer oocytes than their control counterparts. Artifacts of surgical stress or vascular diffusion of serine protease inhibitor from treated to control sides were ruled out by appropriate control experiments. We conclude that early serine protease inhibitor treatment of pregnant mare serum gonadotropin-stimulated rat ovaries impairs folliculogenesis. Thus, in addition to involvement in ovulation, serine proteases appear to play important roles throughout follicular development.

Aminocaproic Acid↗
PubMed2004

Direct injection of vascular endothelial growth factor into the ovary of mice promotes follicular development.

OBJECTIVE: To investigate the effects of an ovarian injection of vascular endothelial growth factor (VEGF) on antral follicle development, neoangiogenesis, and apoptosis. DESIGN: Controlled laboratory study. SETTING: University-affiliated fertility center. ANIMAL(S): Balb/c female mice (n = 32) were studied. INTERVENTION(S): Mice were divided into four groups: control group (C) n = 6, no treatment; hyperstimulated group (HS), n = 8, ovaries were stimulated with 7.5 IU pregnant mare serum gonadotropin (PMSG) and 10 IU of hCG; VEGF group (V), n = 8, injected with 0.1 mL of VEGF (0.2 microg) in each ovary; V+HS, n = 8 injected with VEGF and 2 weeks later hyperstimulated. MAIN OUTCOME MEASURE(S): Number of antral and luteinized follicles, number of vessels, and percentage of Bcl-2-positive cells. RESULT(S): The number of antral follicles with VEGF was higher than in the C and HS groups (16.0 +/- 2.5 vs. 6.0 +/- 0.9 and 11.3 +/- 0.6, respectively, p<0.005). All treatments significantly increased the number of vessels (C: 5.0 +/- 0.5 vs. V: 20.0 +/- 4.8, p<0.005 and V+HS: 22.2 +/- 1.2, p<0.01), as well as increased Bcl-2-positive cells compared to controls (C: 0; V: 11.8 +/- 3.5, p<0.005; V+HS: 12.5 +/- 3.7, p<0.005). CONCLUSION(S): Our findings demonstrated that a direct injection of VEGF into the mouse ovary results in the development of an enhanced vascular network promoting follicular development and diminishing apoptosis.

Animals↗
PubMed1985

Ovarian sympathectomy in the golden hamster: effects on estrous cyclicity and follicular development.

The role of adrenergic nerves in estrous cyclicity and follicular growth was studied in sympathectomized hamster ovaries. Specific ovarian sympathectomy was accomplished by injection of 6-hydroxydopamine (6-OHDA) into the ovarian bursal sac. Ovarian sympathectomy abolished all fluorescent adrenergic nerves 4, 8 or 12 days after treatment. Bilateral ovarian sympathectomy on metestrus altered the first estrous cycle in 53% of the animals and 20% had an altered second cycle. All sham injected animals had normal cycles. Four days after sympathectomy, there was a decrease in healthy follicles 80-240 microns and 250-340 microns in diameter and increased atresia of follicles 80-240 microns and 350-440 microns in diameter compared to solvent treated ovaries. Bilateral 6-OHDA treatment did not affect ovarian weight, number of corpora lutea or the total number of follicles per ovary. These observations suggest that ovarian adrenergic nerves modulate healthy follicular development in the golden hamster.

Animals↗