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W G Rossmanith

Publications and source records attributed to W G Rossmanith.

At least 73 records · Page 4Linked to original sources
PubMed1991

The luteinizing hormone pulsatile secretion: diurnal excursions in normally cycling and postmenopausal women.

While numerous investigations have determined characteristics of episodic luteinizing hormone (LH) secretion in women, any diurnal LH rhythmicities during eugonadal and hypogonadal states have not been accurately addressed. Accordingly, blood was sampled at 15-min intervals for 24 h in 45 normally cycling women (16 early follicular (EFP), 14 late follicular (LFP), 15 mid-luteal phase (MLP) women) and in eight postmenopausal women (PMW). Pulse attributes (amplitudes, interpulse intervals) determined in the LH secretory profiles were fitted to cosinor functions to assess diurnal variabilities. In both eugonadal women and PMW, significant (p less than 0.05 or less) diurnal excursions were observed in mean LH levels, with maximal acrophase amplitudes occurring in the EFP and MLP. While these 24-h swings peaked at comparable times (11.00-17.00) during the menstrual cycles, a significant (p less than 0.001) shift in acrophase times to early morning hours (05.30) was noted for PMW. Significant (p less than 0.05 or less) 24-h periodicities were also found for the LH pulse amplitudes. LH pulses were of greater magnitudes during night hours in both cycling women and PMW. A slowing of LH pulses (p less than 0.05 or less) was noted during sleep in EFP and, distinctly, in MLP women. These observations demonstrate diurnal variations in LH secretion and its pulsatile attributes in eugonadal women. Differences in time course and magnitude of these diurnal excursions may be explained by variations in the sex steroid environments. In turn, steroids may modulate other neuroendocrine determinants regulating central time-keepers.

Aged↗
PubMed1991

[Neuroendocrine control of human reproduction. The role of dopaminergic neurotransmitter systems].

By affecting central hypothalamic processes, the dopaminergic neuronal system governs episodic gonadotropin secretion. Serum gonadotropin profiles as an indirect reflection of central activity can consecutively indicate dopaminergic neurotransmitter activity and its changes by pharmacologic manipulation. Despite vigorous efforts, the role of dopamine in the neuroendocrine control of human reproduction remained contentious. Controversial effects of dopamine on gonadotropin discharge have been observed, presumably a result of different experimental conditions. As yet, numerous investigations have not convincingly evidenced a critical role of dopamine in the regulation of the human menstrual cycle. Since central neuroendocrine mechanisms may not be reduced to action of the dopaminergic system, a complexity of hypothalamic dopaminergic interactions with various neurotransmitters and reproductive hormones should be considered to operate in the biochemical control of the central pulse generator activity.

Dopamine↗
PubMed1990

Relative changes in LH pulsatility during the menstrual cycle: using data from hypogonadal women as a reference point.

The basic premise of this study is that the GnRH-LH pulsatile activity, particularly its frequency characteristics, constitutes, in the absence of any considerable ovarian feedback, the intrinsic rhythm of the hypothalamic-pituitary unit at its maximal rate. Thus, LH pulse attributes determined in postpubertal hypogonadal subjects may be used as a reference in assessing the degree of influence exerted by endocrine factors that modulate GnRH-LH pulses. Accordingly, serum LH levels were determined in samples obtained at 15-min intervals for 24 h in 20 hypogonadal women: 13 postmenopausal women (PMW) and seven women with premature ovarian failure (POF). Similar measurements were performed in 60 normally cycling women: 25 in the early follicular phase (EFP), 13 in the late follicular phase (LFP), seven at midcycle surge (LH surge) and 15 in the midluteal phase (MLP). Significant pulses were identified by the cluster algorithm utilizing factors appropriate for 24 h data series of a sampling frequency of 15-min intervals. The results show a 24-h mean (+/- SE) LH pulse frequency of 78.2 +/- 2.8 and 85.5 +/- 2.4 min per pulse for young (POF) and older (PMW) hypogonadal women, respectively. During the follicular phase of the cycle, the LH pulse frequency is not significantly different from that of hypogonadal women, but there is a significant (P less than 0.05) increase from early to late follicular phases (95.4 +/- 3.3 vs 78.8 +/- 2.2 min per pulse). However, when the sleep periods are excluded from the 24-h data series because of the associated decrease of LH pulse frequency in EFP women, the resulting pulse frequencies are almost identical for EFP, LFP and PMW. An elevation beyond the basic pulse rhythm determined in PMW or POF is not observed in any phase of the menstrual cycle studied, including the midcycle surge. The decrease in LH pulse frequency during the luteal phase of the cycle (151.8 +/- 8.0 min per pulse, P less than 0.001 vs hypogonadal women) beyond the reference pulse frequency of hypogonadal women is unequivocal. By contrast, the pulse amplitude varies markedly among the groups with the largest found in POF (36.6 +/- 4.5 IU/l). It follows, in descending order, PMW (22.7 +/- 3.1 IU/l), midcycle surge (17.3 +/- 2.8 IU/l), MLP women (7.0 +/- 1.3 IU/l) and the EFP (4.9 +/- 0.3 IU/l) and LFP (4.0 +/- 0.4 IU/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Secretory dynamics of oestradiol (E2) and progesterone (P4) during periods of relative pituitary LH quiescence in the midluteal phase of the menstrual cycle.

Although the temporal relationship between pulsatile pituitary luteinizing hormone (LH) secretion and steroid hormone release from the corpus luteum has been investigated, the secretory profiles of oestradiol (E2) and progesterone (P4) during periods without any discernible LH pulsatile activity remain unknown. Consequently, blood was sampled at 15-min intervals for 24 h from 16 women during the midluteal phases (6-8 days after midcycle LH surge) of their cycles. LH was measured in all samples and analysed for significant pulses by the Cluster pulse algorithm. Nine studies showing the lowest LH pulse frequencies and large LH pulse amplitudes were also assessed for E2 and P4 in all samples. All three hormones were released in pulsatile fashions. Pulses of E2 and P4 were found to be synchronous. While the release frequencies for E2 (mean +/- SEM: 8.9 +/- 0.7 pulses/24 h) and P4 (8.5 +/- 0.7 pulses/24 h) were comparable, the LH pulse frequency (4.6 +/- 0.4 pulses/24 h) was found to be significantly (P less than 0.001) lower than the ovarian steroid pulse frequencies. Maximum (P less than 0.01) cross-correlation coefficients were determined at positive time lags of 28.1 +/- 7.7 min for LH/E2 and 31.7 +/- 5.8 min for LH/P4, indicating that changes in E2 or P4 levels tended to occur within approximately 30 min following LH concentration changes. Further, the degree of concomitance between a steroid pulse and an LH peak was much higher (P less than 0.001) than by chance. Maximum (P less than 0.01) cross-correlation coefficients between E2 and P4 hormonal data series were found at zero time lag, suggesting that these sex steroids were secreted simultaneously. The pulse amplitudes, pulse durations and areas under the peaks of those E2 or P4 pulses preceded by large (greater than 5 IU/l) amplitude LH pulse were significantly greater (P less than 0.05 or less for all comparisons) than for steroid pulses not associated with preceding LH pulses. Thus, two populations of steroid pulses were observed; one associated with preceding LH pulses and having greater magnitude of all pulse attributes (duration, amplitude, area under the peaks), and another, not associated with preceding LH pulses and having pulse characteristics of lower magnitude. This observation suggests that the pulsatile release of ovarian steroids is a result of the episodic modulating influence of LH and that pulsatile steroid hormone secretion pertains with smaller magnitude during periods of relative pituitary quiescence of LH pulsatility.

Adult↗
PubMed1990

Pulsatile GnRH-stimulated LH release from the human fetal pituitary in vitro: sex-associated differences.

An in-vitro perfusion system was utilized to examine LH release from human fetal (19-24 weeks gestation) anterior pituitaries during repetitive GnRH stimulations. Pituitaries (five male, four female) were dissected into halves, and one hemipituitary of each pair was stimulated with 10-min pulses of 1 nM GnRH administered at 60-min intervals over 24h, whereas the matching hemipituitary received pulses of medium alone. Basal (no GnRH stimulation) LH release from female hemipituitaries was significantly (P less than 0.01) greater than from male hemipituitaries, and the amplitude of LH release associated with GnRH pulses was sixfold greater (P less than 0.001) with female hemipituitaries. Furthermore, the magnitude of LH release associated with individual GnRH pulses was significantly (P less than 0.001) enhanced during the course of female hemipituitary perfusions, but not during perifusion of male hemipituitaries. These studies demonstrate that LH secretion by the female, but not male, mid-gestational human fetal pituitary is increased in response to a physiological pattern and interval of repeated pulsatile GnRH stimulation in vitro.

Female↗
PubMed1990

Pulsatile cosecretion of estradiol and progesterone by the midluteal phase corpus luteum: temporal link to luteinizing hormone pulses.

Using recently defined analytical tools that permit quantitative and integrated assessments of pulsatile activities of two or more hormones, we have examined the coincidence of pulses of estradiol (E2), progesterone (P4), and LH determined in blood withdrawn at 15-min sampling intervals for a duration of 24 h in each of 15 women during the midluteal phase of the human menstrual cycle. The occurrence of E2 and P4 pulses is simultaneous, as their peaks were maximally correlated at zero time lag (P less than 10(-4], and there were comparable periodicities for E2 (13.5 +/- 0.7 pulses/24 h) and P4 (11.2 +/- 0.7 pulses/24 h). This coupling of E2 and P4 pulses suggests cosecretion by the mature corpus luteum. These E2 and P4 pulses are significantly coupled with LH pulses, with a lag time of about 30 min and/or 45 min for P4 (P = 0.029) and 0 min and/or 15 min for E2 (P = 0.032). Further, when considered together, LH, E2, and P4 are found to be triply copulsatile (P = 0.0066). However, significant numbers of discrete pulses of P4 and E2 are observed without antecedent LH pulses, suggesting some degree of corpus luteum autonomy. In conclusion, orchestrated synchrony of pulsatile pituitary and ovarian (corpus luteum) signaling can be demonstrated by the coordinated temporal release of LH, E2, and P4 in normal cycling women.

Adult↗
PubMed1989

The effects of prolonged opioidergic blockade on LH pulsatile secretion during the menstrual cycle.

Although considerable evidence points towards a pivotal role for the endogenous opioid peptides (EOP) in the neuroendocrine regulation of GnRH-LH secretion, the effects of prolonged opioidergic blockade on LH pulsatile activity during the menstrual cycle have not been thoroughly investigated. Accordingly, 10 women in the early follicular phase (EFP, days 3 and 4), 10 women in the late follicular phase (LFP, days 9 to 13) and 7 women in the midluteal phase (MLP, days 6 to 8 after LH surge) were studied on two consecutive days before and during opioidergic blockade imposed by an opiate receptor antagonist, naloxone. Blood samples were obtained at 15 min intervals for 8 h during saline (150 mmol/l at 50 ml/h) or naloxone (30 micrograms/kg/h) infusions. Furthermore, sequential 24-h infusions of saline or naloxone (30 micrograms/kg/h) were performed in 6 other women (two each in the EFP, LFP, and MLP). LH hormone series were analyzed for significant pulses by the Cluster pulse algorithm. While 8-h naloxone infusions did not change any of the LH pulse characteristics (frequency, amplitude, transverse mean, duration) in the EFP, they elevated significantly (p less than 0.05) the LH pulse frequencies, pulse amplitudes and transverse mean levels in the LFP. In the MLP, the LH pulse amplitudes were significantly (p less than 0.05) increased, but pulse frequencies and transverse mean levels remained unchanged. While the 24-h naloxone infusions did not alter any of the pulse characteristics in the EFP, they elicited a robust increase in LH pulsatile activity in the LFP, composed of a progressive rise in LH pulse amplitudes and transverse mean levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Does prolonged dopaminergic blockade alter the LH pulsatile secretion in normal cycling and postmenopausal women?

To investigate effects of prolonged dopaminergic antagonism on LH pulsatile secretion, 22 normal cycling women (10 in the early follicular phase (days 3 and 4), 6 in the late follicular phase (days 10 to 13), 6 in the midluteal phase (days 6 to 8 after ovulations) and 8 postmenopausal women were studied before and during 8-h dopamine receptor blockade imposed by metoclopramide. Sequential 8-h infusions of either saline (50 ml/h) or metoclopramide (30 micrograms . kg-1 . h-1) were conducted on two consecutive days. LH pulsatile activity was assessed in blood samples obtained at 15 min intervals during these 8-h infusion periods. Based estradiol and progesterone concentrations were lowest (p. less than 0.001) in postmenopausal and highest (p less than 0.001) in the midluteal phase women, 8-h metoclopramide infusions evoked prompt (within 90 min, p less than 0.001) and sustained (greater than 70 micrograms/l, p less than 0.001) increases of PRL, similar (p = 0.78) in magnitude for normal cycling and postmenopausal women. Metoclopramide infusions failed to significantly modify the LH pulsatile activity during the menstrual cycles and in hypogonadal women. These observations suggest that even in the presence of high circulating estradiol and progesterone concentrations the dopaminergic inhibition may not be operating. However, any possible stimulatory effect on LH secretion by dopamine receptor blockade may be confounded by the concomitant metoclopramide-induced hyperprolactinemia.

Adult↗
PubMed1989

Endocrine dynamics during pulsatile GnRH administration in patients with hypothalamic amenorrhea and polycystic ovarian disease.

The LH secretory patterns and ovarian endocrine responses have been determined during pulsatile gonadotropin-releasing hormone (GnRH) administration for induction of ovulation in patients with hypothalamic amenorrhea (HA). However, until now these endocrine dynamics during GnRH therapy have not been thoroughly investigated in patients with polycystic ovarian disease (PCOD). Seven patients with HA and 4 patients with PCOD have therefore been studied to determine changes in LH pulsatile activity and in serum sex steroid levels in response to chronic intermittent GnRH stimulation. GnRH was administered intravenously (5-10 micrograms/90 minutes) by means of a portable infusion pump. Blood samples were obtained at 15-minute intervals for 4 hours on the day before the start of GnRH stimulation (control day) and on treatment days 5, 10 and 15. LH was determined in all samples and FSH, serum androgens and estrogens were measured in baseline samples by RIA. While 8 (62%) ovulations and 5 conceptions were observed in 13 treatment cycles in patients with HA, no ovulations were achieved during 9 treatment cycles in patients with PCOD. On the control day significantly (p less than 0.05) higher basal LH and testosterone (T) levels and significantly (p less than 0.05) lower FSH levels were found in the PCOD patients. The LH pulsatile profiles of the PCOD patients showed significantly (p less than 0.05) higher pulse amplitudes and areas under the curve (integrated responses). Pulsatile GnRH administration induced a significant (p less than 0.05) increase in LH pulse amplitudes in both HA and PCOD patients, and also increased (p less than 0.05) the integrated responses in patients with HA. During the GnRH stimulation, the LH interpulse intervals of both HA and PCOD patients were found to be similar to the frequency in which exogenous GnRH was administered. FSH levels rose continuously (p less than 0.001) during stimulation in patients with HA, but remained unchanged in patients with PCOD. In HA patients, T, androstenedione (AD) and estrone (E1) did not change during the GnRH treatment, but estradiol (E2) rose so that the ratios of aromatized estrogens to non-aromatized androgens (E1/AD, E2/T) increased. In contrast, T and AD increased significantly (p less than 0.05 or less) and E2 remained unchanged during stimulations in PCOD patients, which resulted in decreasing ratios of estrogens to androgens. These observations confirm that pulsatile GnRH administration can successfully induce ovulation in patients with HA by restoring the ovarian physiology. The data also demonstrate that pulsatile GnRH administration can influence the LH secretory patterns in PCOD patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Effects of acute hyperprolactinemia on LH pulsatile secretion in hypogonadal and early follicular phase women.

To investigate the effects of acute hyperprolactinemia on the 24 h LH pulsatile pattern, 11 women in the early follicular phase (EF, days 3 and 4) and 8 postmenopausal women (PMW) were studied before and during administration of metoclopramide, a dopamine receptor antagonist. Sequential 24 h infusions of either metoclopramide (MCP, 30 micrograms/kg/h) or normal saline were conducted and pulsatile LH activity assessed for 48 hrs. In both EF women and PMW, a prompt (within 90 min, p less than 0.001) and sustained (greater than 45 micrograms/L, p less than 0.001) release of PRL was induced by MCP infusions. MCP-induced hyperprolactinemia failed to modify the LH pulsatile activity in both EF women and PMW. These observations suggest that acute hyperprolactinemia due to dopaminergic blockade has no discernible effect on LH pulsatility and that the reduced LH pulse frequency observed in association with endogenous hyperprolactinemia may result from different neuroendocrine mechanism(s) and/or is time dependent.

Adult↗
PubMed1988

Effects of dopaminergic blockade on the sleep-associated changes of luteinizing hormone pulsatility in early follicular phase women.

To investigate the dopaminergic role in the sleep-associated changes of luteinizing hormone (LH) pulsatile pattern, 11 normal cycling women were studied in the early follicular phase (EF, days 3 and 4) of their cycles before and after the administration of metoclopramide (MCP), a dopamine receptor antagonist. Twenty-four-hour infusions of either saline (NaCl 150 mmol/1-50 ml/h) or metoclopramide (MCP, 30 micrograms/kg/h) were conducted in a random sequence. Pulsatile LH activities were assessed in blood samples obtained at 15-min intervals for 48 h. Sleep was electrophysiologically confirmed by EEG during night hours (23.00-07.00 h). Significant sleep-associated decreases in LH pulse frequency (p less than 0.05) and mean LH serum levels (p less than 0.001) with a concurrent increase in LH pulse amplitude (p less than 0.01) were observed during the saline control studies. MCP infusion failed to significantly modify the LH pulsatile activity during either the wake or sleep periods. In particular, it did not prevent the changes in LH pulsatility during sleep. This observation suggests that a dopaminergic mechanism does not critically contribute to the sleep-related changes in LH pulsatile activity in women during the early follicular phase.

Adult↗
PubMed1988

Dopaminergic control of circadian and pulsatile pituitary thyrotropin release in women.

Dopamine (DA) inhibits pituitary TSH release, but its role as a regulator of circadian and pulsatile TSH secretion is not clear. Accordingly, we studied the 24-h TSH secretory patterns in seven normal women in the early follicular phase of their cycles before and during DA receptor blockade by metoclopramide (MCP). Serum TSH was measured by a highly sensitive (0.05 mU/L) RIA at 15-min intervals for 48 h during sequential 24-h saline and 24-h MCP infusions (30 micrograms/kg.h). Sleep was confirmed by electroencephalogram between 2300-0700 h. All women had a nocturnal rise of TSH, independent of sleep, which began in the late afternoon and reached a peak (acrophase) after midnight during the saline infusion. This circadian periodicity was composed of a series of TSH pulses with greater magnitude and frequency during nocturnal hours. Infusion of MCP had no effect on pulse frequency, but the pulse amplitude increased (P less than 0.05), especially at night. As a consequence, the circadian excursion of TSH, as assessed by cosinor function, was exaggerated. The mean acrophase amplitude and mesor levels increased (P less than 0.05), but the nadir and acrophase times did not change. These findings suggest that DA is an inhibitor of TSH pulse amplitude throughout the 24-h biological clock. By inference, the neuroendocrine mechanism(s) that underlies the nocturnal increase in TSH secretion is not due to decreased dopaminergic inhibition.

Adult↗
PubMed1988

Role of endogenous opioid peptides in the initiation of the midcycle luteinizing hormone surge in normal cycling women.

While compelling evidence indicates a pivotal role for endogenous opioids in the regulation of GnRH-LH pulsatile activity during the late follicular and luteal phases of the menstrual cycle, the participation, if any, of the opioidergic mechanism in the initiation of the midcycle surge has not been examined. Accordingly, we measured serum LH, FSH, estradiol (E2) and progesterone (P4) levels daily during 2 consecutive cycles in 12 normal cycling women. After a control cycle, each woman was infused with naloxone (30 micrograms/kg.h) for 24 h starting 3 days before the anticipated spontaneous midcycle surge. Blood samples were obtained at 15-min intervals for 8 h before, during, and 16 h after the naloxone infusion. Serum LH and FSH concentrations were measured in all samples, and serum E2 and P4 concentrations at 2-h intervals. Pulsatile LH secretion was analyzed using the cluster program. The opioidergic blockade elicited a robust increase in LH pulsatile activity and a 3-fold rise in serum FSH levels in 6 of the 12 women. This increased gonadotropin secretion lasted more than 24 h and was characterized by a progressive increase in LH pulse amplitude, which was 9-fold greater during the last 8 h of naloxone infusion [mean LH pulse amplitude, 36.5 +/- 4.5 (+/- SE) vs. 4.1 +/- 0.4 IU/L; P less than 0.001]. This increase was accompanied by a corresponding increase in transverse mean serum LH levels (83.3 +/- 13 vs. 20.7 +/- 3.2 IU/L; P less than 0.001), but no alteration of the interpulse interval (93 +/- 11 vs. 85 +/- 4 min). The peak serum LH concentrations exceeded 100 IU/L in all 6 of these women. This naloxone-advanced gonadotropin surge, resembling closely the spontaneous midcycle surge, resulted in a significantly shortened (P less than 0.001) follicular phase and a more than 2-fold elevation of serum P4, followed by assumed ovulation and normal luteal function. These 6 women had serum E2 levels immediately before naloxone infusion that were comparable to those during the preovulatory peak during the control cycle. In the 6 women who did not have a naloxone-induced increase in gonadotropin secretion the preinfusion serum E2 levels were substantially lower (P less than 0.001) than the values during the control cycle. These findings suggest that a transient decrease in opioidergic activity may contribute to the initiation of the midcycle gonadotropin surge in women.

Adult↗