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At least 343 records · Page 19Linked to original sources
PubMed1976

Response of plasma LH and FSH to synthetic LH-RH in children at various pubertal stages.

Fifty normal boys and 47 normal girls, aged 5 to 18 years, underwent a standard luteinizing hormone-releasing hormone (LH-RH) test (50 mug/sq m by rapid intravenous injection), and the plasma levels of LH and follicle-stimulating hormone (FSH) were determined. The results were analyzed separately according to the pubertal stages for each sex. A wide range of distribution of the individual measurements of the plasma gonadotropins throughout the LH-RH tests was found, but the mean values of the basal and peak levels showed a definite pattern for each sex at the different pubertal stages. Of particular interest was the sharp rise in basal plasma FSH level and its marked response to LH-RH in girls at the onset of puberty. The girls at this stage had the highest basal and peak FSH levels obtained at any pubertal stage in both sexes. It is concluded that the establishment of norms of LH and FSH response to a standard dose of LH-RH will be useful in evaluating normal and abnormal pubertal states in both sexes.

Adolescent↗
PubMed1980

Interaction of the anti-estrogen CI-628 and estradiol on plasma LH and hypothalamic LH-RH in the female rat.

The effects of the anti-estrogen Ci-628 have been tested on both plasma LH and hypothalamic LH-RH content in ovariectomized or ovariectomized, estradiol (E2)-implanted rats, in order to correlate those parameters with the [3H]E2 retention in the hypothalamus and the pituitary. Incresing doses of CI-628 induced a dose-dependent inhibition of [3H]E2 retention in both cytosolic and nuclear fractions of the pituitary. In contrast, hypothalamic retention of [3H]E2 is only inhibited significantly with higher doses of CI-628 (2.4 and 24 mg/kg). In ovariectomized rats, only a high dose of CI-628 (24 mg/kg) is able to decrease elevated LH levels observed following castration. In the presence of E2, CI-628 has both estrogenic and anti-estrogenic properties on LH secretion. CI-628 acts at the pituitary level to decrease the tissue sensitivity to LH-RH, but has no effect on mediobasal hypothalamic (MBH) LH-RH content.

Animals↗
PubMed1988

The release of pituitary LH and sprouting of LH-releasing hormone (LHRH)-containing neurons after anterior hypothalamic deafferentation.

The chronology of changes in plasma luteinizing hormone (LH) and the distribution of immunoreactive neuronal processes containing LH releasing hormone (LHRH-ir) were studied in the female rat after surgical interruption of anterior neural connections of the mediobasal hypothalamus (MBH). Spontaneous LH surges on the afternoon of proestrus and LH release after estradiol benzoate (EB) followed 48 h later by progesterone (P) administration were studied in ovariectomized (OVX) rats. The maximum increase in plasma concentrations (delta maxLH) after EBP was calculated for each rat at several intervals over 140 days. Control animals given EBP at monthly intervals after OVX had comparably large delta maxLH surges during the first few months of study. However, a gradual decline in control delta maxLH followed becoming significant 3 months after the start of the experiment. In contrast, frontal cuts (FC), which interrupted anterior MBH connections, produced an abrupt decrease in delta maxLH surges after EBP to 11% of preoperative levels. However, during subsequent EBP trials, there was a gradual improvement in LH surges to about 50% of preoperative levels over 100 days. In some cases, individual improvement became equal to preoperative LH surge levels, in others there was no recovery. Examination of LHRH-ir nerve fiber growth responses after FC suggested that sprouting by these peptide-containing neuronal processes may have contributed to the functional improvements observed.

Animals↗
PubMed1981

GnRH induced LH release in suckled beef cows. 1. The effects of days postpartum and estradiol-17beta concentrations on the release of LH following administration of GnRH.

Twenty suckled CharloixxHereford beef cows (5 cows/group) were assigned at random to receive 100 microg GnRH (IM) at either 2 to 3, 7 to 8, 15 to 16, or 31 to 32 days postpartum, Groups 1 through 4, respectively. Blood samples for hormone determinations were collected at time 0 (pre-GnRH), every half hr for 3 hr, and at 4.0 hr and 6.0 hr post-GnRH. Mean plasma LH, estradiol-17beta, or progesterone concentrations were not different among groups prior to GnRH. Plasma LH increased (P<.05) following GnRH in Groups 2, 3 and 4, but not in Group 1. Peak GnRH induced LH release was greater (P<.05) in Groups 3 and 4 than in Groups 1 or 2. Correlation coefficients between days postpartum and peak LH release (r=.72), and estradiol-17beta concentrations and time of LH peak (r=-.42) were significant (P<.05). These data indicate that LH release in response to GnRH, in suckled beef cows is not fully restored until 15 to 16 days postpartum.

Journal Article↗
PubMed1995

Administration of human chorionic gonadotropin for in vitro fertilization-embryo transfer based on the serum luteinizing hormone (LH) concentration: the importance of synchronization with endogenous LH rises.

OBJECTIVE: To examine whether synchronized administration of hCG at the onset of the endogenous LH rise promotes successful IVF. DESIGN: A prospective randomized study. SETTING: In vitro fertilization program at a university hospital. PATIENTS: A total of 208 IVF cycles in 148 patients. INTERVENTIONS: Serum LH concentrations were measured daily and hMG was administered daily. Independent of follicle size and E2 concentration, hCG was administered as soon as the LH concentration exceeded the J level, defined as the minimum value + (the day 3 value-the minimum value) x 1/3(J group). Alternatively, hCG was administered when the serum LH concentration turned to increase but was still less than the J level, or 1 day after the serum LH concentration exceeded the J level (non-J group). RESULTS: The rates of total and ongoing pregnancy per cycle were significantly higher in the J group (35.6% and 26.0%, respectively, n = 104) than in the non-J group (21.2% and 12.5%, respectively, n = 104). Pregnancies in the J group were achieved over a wide range of dominant follicle diameters (13 to 25 mm), E2 levels (198 to 1,700 pg/mL; conversion factor to SI units, 3.671), and E2 level per follicle > or = 12 mm (24 to 225 pg/mL per follicle) recorded on the day of hCG administration. CONCLUSION: Synchronized administration of hCG in accordance with endogenous LH rises produces a high rate of pregnancy in IVF.

Adult↗
PubMed1996

Reduction of the amplitude of preovulatory LH and FSH surges and of the amplitude of the in vitro GnRH-induced LH release by substance P. Reversal of the effect by RP 67580.

The effects of Substance P (SP) and of a specific nonpeptide antagonist of the NK1 receptor (RP 67580) on preovulatory gonadotropin surges and on the in vitro GnRH induced LH surge were investigated in cycling female rats. A subcutaneous injection of SP (0.5 mg/kg body weight) at 12.00 h on the proestrous day significantly decreased the LH preovulatory surge. RP 67580 (1.5 mg/kg) significantly increased this LH surge. However, when SP and its antagonist were administered together, LH preovulatory surge was normal. The FSH preovulatory surge at 18.00 h and also at 19.00 h was significantly inhibited by SP administration. RP 67580 alone had no effect on the FSH preovulatory surge. When SP and RP 67580 were both administered, there was no diminution of FSH plasma levels at 18.00 h and 19.00 h. In vitro perifusions of anterior pituitaries showed that SP inhibits GnRH-induced LH release via a NK1 receptor. Thus, SP inhibits the LH preovulatory surge via NK1 receptors and SP modulation of gonadotropin surges is at least partly exerted at the pituitary.

Analysis of Variance↗
PubMed1996

The concentration of GnRH in hypothalamus, LH and FSH in pituitary, LH, PRL and sex steroids in peripheral and ovarian venous plasma of hypo- and hyperthyroid, cysts-bearing gilts.

The aim of this work was to investigate the hormonal pattern in hypo- and hyperthyroid gilts with experimentally induced cystic ovarian disease (COD). A total of 70 adult, nulliparous gilts divided into six groups were used for the experiment. Group I was euthyroid and control. Group II was made hypothyroid by oral administration of methylthiouracyl for 24 days. Group III represented euthyroid gilts injected with gonadotropins (PMSG and hCG). Group IV consisted of hypothyroid gilts injected with gonadotropins. Group V was treated with L-thyroxine for 24 days and Group VI with thyroxine and with gonadotropins for the last 10 days of the test. The treatment of all groups was terminated on the 4th-5th day of the next estrous cycle. The peripheral blood of the gilts was collected on Day 0, and on Day 24. On the 25th day the gilts were laparotomized and cannulas were inserted into utero-ovarian veins of each ovary for blood collection. Simultaneously, peripheral blood samples were collected during 1 to 3 consecutive days. The animals were then slaughtered and the hypothalamus, pituitary and ovaries were frozen and preserved for further analyses. In hypothalamic tissue the content of GnRH: in the pituitary the concentration of LH and FSH; and in peripheral and ovarian blood plasma the level of LH, PRL, E1, P4, A4, T and cortisol (Cl) were estimated by RIA procedure. The level of GnRH in the hypothalamus, and LH and FSH in the pituitary showed a tendency to parallel with thyroid function which may indicate a role of this gland in their production or secretion. In hypothyroid animals an increase of LH and PRL and a slight decrease of secretory function of the ovaries were noted. Injections of gonadotropins in euthyroid or hypo- and hyperthyroid gilts intensified the function of the ovaries, which was manifested by numerous follicular cysts and corpora lutea. The hormonal milieu of gilts from these groups showed a low level of LH, PRL and an increased content of sex steroids in peripheral and ovarian blood. The ovarian steroidogenesis of cyst-bearing gilts was disturbed, which was indicated by an increased level of E1, P4, A4, T, and Cl, but a low level of E2. These disturbances in steroidogenesis in cystic gilts may be caused by a deficiency in LH secretion as the consequence of the pituitary gonadotropin suppression by the used gonadotropins. The steroid hormone pattern of cyst-bearing gilts strongly resembles the endocrine profile noted in polycystic ovarian disease in women.

Animals↗
PubMed2003

Gene expression profiling of human endometrial receptivity on days LH+2 versus LH+7 by microarray technology.

In humans, embryonic implantation and reproduction depends on the interaction of the embryo with the receptive endometrium. To gain a global molecular understanding of human endometrial receptivity, we compared gene expression profiles of pre-receptive (day LH+2) versus receptive (LH+7) endometria obtained from the same fertile woman (n = 5) in the same menstrual cycle in five independent experiments. Biopsies were analysed using the Affymetrix HG-U95A array, a DNA chip containing approximately 12,000 genes. Using the pre-defined criteria of a fold change >/=3 in at least four out of five women, we identified 211 regulated genes. Of these, 153 were up-regulated at LH+7 versus LH+2, whereas 58 were down-regulated. Amongst these 211 regulated genes, we identified genes that were known to play a role in the development of a receptive endometrium, and genes for which a role in endometrial receptivity, or even endometrial expression, has not been previously described. Validation of array data was accomplished by mRNA quantification by real time quantitative fluorescent PCR (Q-PCR) of three up-regulated [glutathione peroxidase 3 (GPx-3), claudin 4 (claudin-4) and solute carrier family 1 member 1 (SLC1A1)] genes in independent LH+2 versus LH+7 endometrial samples from fertile women (n = 3) and the three up-regulated genes throughout the menstrual cycle (n = 15). Human claudin-4 peaks specifically during the implantation window, whereas GPx-3 and SLC1A1 showed highest expression in the late secretory phase. In-situ hybridization (ISH) experiments showed that GPx-3 and SLC1A1 expression was restricted to glandular and luminal epithelial cells during the mid- and late luteal phase. The present work adds new and important data in this field, and highlights the complexity of studying endometrial receptivity even using global gene-expression analysis.

Adult↗
PubMed1995

From basal luteinizing hormone (LH) concentrations to the pre-ovulatory LH surge: titration of the physiological effect of gonadotrophin surge-inhibiting/attenuating factor.

Pulsatile luteinizing hormone (LH) release is thought to be controlled by the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the putative ovarian factor gonadotrophin surge-inhibiting/attenuating factor (GnSIF/AF). Our experiments were designed to titrate the input of endogenous basal and follicle stimulating hormone (FSH)-stimulated GnSIF/AF in this system. The effects were studied of five consecutive pulses of GnRH administration (10-250 pmol/pulse/kg rat), 1 h apart, on the self-priming effect in pro-oestrus phenobarbital-blocked rats injected with FSH or saline. In response to the two high pulses of GnRH, a clear GnRH self-priming was demonstrated. However, pulses of 25 pmol GnRH induced only a minor self-priming effect and the LH blood concentrations were within the physiological range. Pulses of 10 pmol GnRH had no effect. FSH suppressed the unprimed LH response and delayed GnRH self-priming by approximately 1 h. Increasing the GnRH pulse frequency of the 25 pmol GnRH pulses from one to three per hour induced pre-ovulatory-like LH surges. The effect was facilitated by ovariectomy to eliminate GnSIF/AF. Thus, the results are consistent with relative inputs of GnRH and GnSIF/AF being responsible for the changes in LH concentration during the ovarian cycle, including the generation of the mid-cycle LH surge.

Animals↗
PubMed1983

Relationship between the preovulatory luteinizing hormone (LH) surge and androstenedione synthesis of preantral follicles in the cyclic hamster: detection by in vitro responses to LH.

Preantral follicles of cyclic hamsters were isolated on proestrus, estrus and diestrus I, incubated for 3 h in 1 ml TC-199 containing 1 microgram ovine luteinizing hormone (LH) (NIH-S22), and the concentrations of progesterone (P), androstenedione (A) and estradiol (E2) determined by radioimmunoassay. At 0900-1000 h on proestrus (pre-LH surge) preantral follicles produced 2.4 +/- 0.3 ng A/follicle per 3 h, less than 100 pg E2/follicle and less than 250 pg P/follicle. At the peak of the LH surge (1500-1600 h) preantral follicles produced 1.8 +/- 0.2 ng P and 1.9 +/- 0.1 A and less than 100 pg E2/follicle. After the LH surge (1900-2000 h proestrus and 0900-1000 h estrus) preantral follicles were unable to produce A and E2 but produced 4.0 +/- 1.0 and 5.0 +/- 1.1 ng P/follicle, respectively. By 1500-1600 h estrus, the follicles produced 8.1 +/- 3.1 ng P/follicle but synthesized A (1.6 +/- 0.2 ng/follicle) and E2 (362 +/- 98 pg/follicle). On diestrus 1 (0900-1000 h), the large preantral-early antral follicles produced 1.9 +/- 0.3 ng A, 2.4 +/- 0.4 ng E2 and 0.7 +/- 0.2 ng P/follicle. Thus, there was a shift in steroidogenesis by preantral follicles from A to P coincident with the LH surge; then, a shift from P to A to E2 after the LH surge. The LH/follicle-stimulating hormone (FSH) surges were blocked by administration of 6.5 mg phenobarbital (PB)/100 g BW at 1300 h proestrus. On Day 1 of delay (0900-1000 h) these follicles produced large quantities of A (2.2 +/- 0.2 ng/follicle) and small amounts of E2 (273 +/- 27 pg/follicle) but not P (less than 250 pg/follicle).(ABSTRACT TRUNCATED AT 250 WORDS)

Androstenedione↗