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Serum LH Concentrations (serum + lh_concentration)

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Ovarian stromal blood flow following clomiphene citrate challenge test in infertile women

JOURNAL OF CLINICAL ULTRASOUND, Issue 7 2008
Ernest Hung Yu Ng MD
Abstract Purpose. To compare ovarian stromal blood flow indices in the follicular phase and after clomiphene citrate (CC) in infertile women. Methods. Pulsatility index (PI), resistance index (RI), and peak systolic blood flow velocity (PSV) of ovarian stromal vessels were determined by spectral Doppler analysis in the early follicular phase and on day 10 after CC. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol concentrations were determined. Results. A total of 69 infertile women were included in the analysis. No significant differences in the average PI, RI, and PSV of ovarian stromal blood flow were demonstrated in the follicular phase and after CC despite a significant increase in serum estradiol concentration after CC. Serum FSH concentration was similar in the follicular phase and after CC, while serum LH concentration was significantly higher after CC. In the right ovary, ovarian stromal blood flow was absent in 13 (18.8%) patients in the follicular phase and in 6 (8.7%) patients after CC, but the difference did not reach statistical significance. In the left ovary, ovarian stromal blood flow was absent in 13 (18.8%) and 12 (17.4%) patients in the follicular phase and after CC, respectively. Conclusion. Ovarian stromal blood flow indices were similar in the follicular phase and after CC. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound, 2008 [source]

Targeted Cytotoxic Analogue of Luteinizing Hormone-Releasing Hormone (LH-RH) Only Transiently Decreases the Gene Expression of Pituitary Receptors for LH-RH

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2002
M. Kovacs
Abstract A cytotoxic analogue of LH-RH, AN-207, consisting of 2-pyrrolinodoxorubicin (AN-201) linked to carrier [D-Lys6]LH-RH, was developed for targeted therapy of cancers expressing LH-RH-receptors. To determine its possible side-effects on the pituitary gland, we investigated the gene expression of pituitary LH-RH-receptors and LH secretion in ovariectomized female and normal male rats after treatment with the maximum tolerated dose of AN-207. The effect of AN-207 on the gene expression of the pituitary GH-RH-receptors and GH secretion was also assessed in male rats. Five hours after a single i.v. injection of AN-207 at 175 nmol/kg, there was a 39,51% decrease in mRNA expression for the pituitary LH-RH-receptors in male and female rats. The carrier, at an equimolar dose, caused a similar reduction (37,39%), whereas the cytotoxic radical AN-201, at an equitoxic dose (110 nmol/kg), produced only a 12,24% decrease (NS) in the mRNA expression of LH-RH-receptors. AN-207 and the carrier analogue induced a comparable 90,100-fold increase in serum LH concentrations in male rats, and the same 12-fold elevation in OVX rats at 5 h. Seven days after treatment with AN-207, the mRNA levels for the LH-RH receptors and the serum LH concentration were back to normal in both sexes. AN-207, the carrier, and AN-201 had no significant effect on the expression of mRNA for GH-RH-receptors in the pituitary. In vitro, a continuous perfusion of pituitary cells with 10 nM AN-207 did not affect the hormone-releasing function of the targeted LH cells or the nontargeted GH cells. Our results demonstrate that cytotoxic LH-RH analogue AN-207, at the maximum tolerated dose causes only a transient decrease in the gene expression of the pituitary LH-RH receptors, and the levels of mRNA for LH-RH receptor fully recover within 7 days. Moreover, the carrier hormone moiety, and not the cytotoxic radical in AN-207 is responsible for this transient suppression. Our findings suggest that the therapy with cytotoxic LH-RH analogues will not inflict permanent damage to pituitary function. [source]

Inhibition by Lipopolysaccharide of Naloxone-Induced Luteinising Hormone Secretion Is Accompanied by Increases in Corticotropin-Releasing Factor Immunoreactivity in Hypothalamic Paraventricular Neurones in Female Rats

JOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2005
D. He
Abstract We have recently reported that lipopolysaccharide (LPS), a bacterial endotoxin, inhibits steroid-induced as well as naloxone-induced luteinising hormone (LH) secretion in ovariectomised oestrogen-primed rats. In the present study, we examined whether corticotropin-releasing factor (CRF) may be involved in the LPS-induced inhibition of LH secretion. Unanaesthetised rats were treated with an intravenous (i.v.) injection of LPS (10 µg) or saline, followed by an i.v. injection of naloxone (20 mg/kg). After sequential blood samples were collected for determination of serum LH concentrations, the brains were fixed and CRF-immunoreactivity was examined histochemically. In control rats receiving saline injections, only a small number of CRF-immunoreactive (ir) cells were found in the parvocellular portion of the hypothalamic paraventricular nucleus (PVN), and naloxone significantly increased serum LH concentrations within 10 min. By contrast, in LPS-treated rats, the number of CRF-ir cells was significantly greater than that in control rats, and the effect of naloxone was completely abolished. In a separate experiment, an intracerebroventricular injection of 5 µg CRF inhibited naloxone-induced LH release, mimicking the effect of LPS. These results suggest that LPS stimulates production of CRF in PVN neurones, which in turn inhibits LH secretion without opioidergic mediation. [source]

Lipopolysaccharide Inhibits Luteinizing Hormone Release Through Interaction with Opioid and Excitatory Amino Acid Inputs to Gonadotropin-Releasing Hormone Neurones in Female Rats: Possible Evidence for a Common Mechanism Involved in Infection and Immobilization Stress

JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2003
D. He
Abstract Acute immobilization stress suppresses naloxone- and N -methyl- d -aspartate (NMDA)-induced, but not gonadotropin-releasing hormone (GnRH)-induced, luteinizing hormone (LH) release in ovariectomized oestrogen-primed rats. To explore whether a common mechanism may underlie inhibition of gonadotropin secretion by various stressors, we examined in the present study the effect of lipopolysaccharide (LPS) on LH release induced by progesterone, GnRH, naloxone and NMDA. The effect of LPS on Fos expression in GnRH neurones was also examined in association with its effect on steroid-induced LH release. Injection of progesterone (1 mg/rat) at noon induced an LH surge in the afternoon in ovariectomized rats pretreated with oestradiol benzoate. In these rats, the majority of hypothalamic GnRH neurones expressed Fos in the evening. Intravenous (i.v.) administration of LPS (10 µg/rat) inhibited steroid-induced LH release and also reduced the Fos expression in GnRH neurones. In separate experiments, an i.v. injection of GnRH (50 ng/kg), naloxone (10 mg/kg) or NMDA (20 mg/kg) significantly elevated serum LH concentrations within 10 min. Pretreatment with LPS, which did not affect basal LH release or GnRH-induced LH release, inhibited naloxone-induced and NMDA-induced LH release. These results show that LPS has a suprapituitary site(s) of action to suppress the activity of GnRH neurones in female rats, and suggest that LPS affects the opioid, as well as the excitatory amino acidergic regulation of GnRH neurones. The similarity of effects of LPS and immobilization stress further suggests that a common mechanism is involved in inhibition of GnRH neurones by different stressors. [source]

Targeted Cytotoxic Analogue of Luteinizing Hormone-Releasing Hormone (LH-RH) Only Transiently Decreases the Gene Expression of Pituitary Receptors for LH-RH

FSH and ovarian response: spontaneous recovery of pituitary,ovarian activity during the pill-free period vs. exogenous recombinant FSH during high-dose combined oral contraceptives

CLINICAL ENDOCRINOLOGY, Issue 4 2002
A. M. Van Heusden
Summary ojbective Compare spontaneous recovery of pituitary,ovarian activity during the pill-free period following the correct use of low-dose oral contraceptives and subsequent ovarian function during the administration of exogenous recombinant FSH (recFSH) after switching to continued Lyndiol® (2·5 mg lynestrenol + 0·05 mg ethinyl-oestradiol) medication. design Prospective, randomized, group-comparative, single-centre study. Following the monitoring of the pill-free period (week 1) and subsequent treatment with Lyndiol® (for a total of 5 weeks), all subjects were randomly allocated to one of four groups receiving daily FSH injections for 1 week [75, 150, 225 IU recFSH or 150 IU purified urinary FSH (uFSH)] during the fourth week of Lyndiol® use. patients Thirty-six healthy volunteers aged 18,39 years, prestudy oral contraceptive use for at least 3 months, cycle length between 24 and 35 days. measurements Serum FSH, LH and oestradiol (E2) concentrations as well as transvaginal ultrasound assessment of the number and diameter of follicles > 2 mm were used to monitor pituitary ovarian function. results At the start of the pill-free period following the prestudy contraceptive medication, 67% of the women presented with LH and FSH levels < 1 IU/l and only one follicle > 10 mm was observed. Initial levels of LH and FSH correlated (P < 0·05) with the extent of pituitary,ovarian activity during the pill-free period. At the end of the pill-free period a follicle > 10 mm had emerged in one subject only. During the first 3 days of Lyndiol® use, seven women (19%) eventually showed at least one follicle > 10 mm. During combined exogenous FSH and Lyndiol® administration, LH levels remained completely suppressed (, 0·5 IU/l) in all women studied. FSH levels and number and size of follicles increased with increasing doses of exogenous FSH in a dose-dependent manner. E2 levels remained low in all groups (< 150 pmol/l). During the week following FSH administration, FSH levels and E2 levels decreased gradually while the number of follicles > 10 mm still increased. conclusions We have confirmed that dominant follicles > 10 mm are present at the end of the pill-free period and during the first days after resumption of pill intake. Once follicles > 10 mm arose at the end of the pill-free period, continued use of Lyndiol® did not reduce follicle diameters. One week of Lyndiol® reduces pituitary,ovarian activity to levels observed after 3 weeks of low-dose pills. FSH administration during Lyndiol® resulted in dose-dependent follicle growth despite extremely low LH levels. E2 secretion (56 ± 51 pmol/l) occurred to a limited and variable extent along with extremely low serum LH concentrations. Recovery of pituitary,ovarian activity at the end of the pill-free period is comparable to FSH levels and follicle dynamics following 7 days of 75,150 IU/l recFSH. [source]