PubMed Health⌕ Search

Biomedical subjects

A Steiger

Publications and source records attributed to A Steiger.

At least 91 records · Page 5Linked to original sources
PubMed1992

Effects of growth hormone-releasing hormone and somatostatin on sleep EEG and nocturnal hormone secretion in male controls.

When applied centrally to animals, growth hormone-releasing hormone (GHRH) stimulates slow-wave sleep (SWS), whereas somatostatin (SRIF) increases REM sleep. We investigated whether these peptides also affect the sleep EEG in humans when given intravenously by comparing polysomnographically the effects of four boluses of (1) placebo, (2) 50 micrograms GHRH or (3) 50 micrograms SRIF administered at 22.00, 23.00, 24.00 and 1.00 h to 7 male controls. In addition, we collected blood samples through a long catheter every 20 min from 22.00 to 7.00 h and measured plasma cortisol and growth hormone (GH) levels. In comparison with SRIF and placebo, GHRH produced a significant increase in plasma GH concentration throughout the night (mean +/- SD: 10.8 +/- 2.0 ng/ml after GHRH; 3.0 +/- 1.7 ng/ml after SRIF and 3.2 +/- 2.0 ng/ml after placebo). SRIF failed to substantially attenuate the nocturnal GH release. Nocturnal cortisol secretion was blunted after GHRH but remained unaffected by SRIF (61.4 +/- 12.9 ng/ml after placebo; 46.6 +/- 19.7 ng/ml after GHRH and 70.8 +/- 12.6 ng/ml after SRIF). Quantitative sleep EEG staging showed a significant increase in SWS after GHRH administration but no change after SRIF (percent spent in SWS per night: 14.0 +/- 5.6 after placebo, 20.2 +/- 6.6 after GHRH and 15.1 +/- 8.2 after SRIF). Application of SRIF was accompanied by a trend toward increased REM density. The effects of episodic GHRH administration upon SWS, GH and cortisol secretion were opposite to those previously reported for corticotropin-releasing hormone, which supports the view that neuroregulation of human sleep involves an interaction of central GHRH and corticotropin-releasing hormone.

Adult↗
PubMed1992

[The importance of applied ethology for the execution of animal welfare legislation].

Applied ethology in general and farm animal ethology in particular have a great importance in connection with animal welfare regulations on a national and international level. They have through the legislation on animal welfare brought about important repercussions on housing of farm animals, wild animals and experimental animals in Switzerland. The animal welfare legislation has been a considerable boost to scientific research. The application of ethological knowledge in the legislation and in practice has indeed also its limits. The importance of applied ethology for animal welfare and for animal husbandry will still increase in future.

Animal Husbandry↗
PubMed1991

Sleep EEG and nocturnal secretion of testosterone and cortisol in patients with major endogenous depression during acute phase and after remission.

Sleep EEG and the nocturnal secretion of cortisol and testosterone in 12 male patients (mean age 46.4 +/- 11.26 years) with major endogenous depression were investigated concomitantly during acute depression, before treatment and after recovery and drug cessation. Testosterone concentration increased after remission, while cortisol secretion decreased. Sleep EEG disturbances remained unchanged in remitted patients. The data suggest that a blunted testosterone and an elevated cortisol secretion are state markers of acute depression, which normalize independently from sleep structure. An interaction between the hypothalamic-pituitary-gonadal axis and the limbic-hypothalamic-pituitary-adrenocortical axis appears likely.

Adult↗
PubMed1991

An interdisciplinary study towards a multiaxial classification of male sexual dysfunction.

The classification of male sexual dysfunction (SD) was investigated in a multidisciplinary study involving a sample of 25 outpatients whose phenomenology, course and biologic comorbidity is described. All 25 patients were suffering from arousal disorders; 9 men complained of lack of desire and 9 of orgasm disorders. For the vast majority (19/25), the arousal disorder preceded the other sexual dysfunctions. Eleven patients suffered from a psychopathological disorder according to DSM-III or DSM-III-R (Axis I and II), with general anxiety, major depression and obsessive-compulsive personality being the most common disorders. Only 6 patients were free of any organic disorder or pathological laboratory finding known to be related to sexual dysfunction. These results served as the basis for analyzing the fit of our data in the most prominent classification systems DSM-III, DSM-III-R, Mainz multiaxial classification model and the traditional dichotomy model. According to our data, the comorbidity of biologic and mental conditions was very high, as most patients (60%) suffered from more than one etiologic factor known to be related to SD. Based on these results, a modification of the DSM-III-R system is suggested.

Adolescent↗
PubMed1989

Examination and treatment of sleep-related painful erections--a case report.

The case of a patient with sleep-related painful erections is described. Insomnia and a slight depressive syndrome occurred along with a long history of this disorder. No physical abnormality was found. At a baseline recording of sleep electroencephalography (EEG) and nocturnal penile tumescence (NPT), a disturbed sleep pattern and impaired NPT were recorded. Attempts to treat the disorder with diazepam, amitriptyline, trimipramine, and biperidene did not prompt a stable improvement of the disorder, but a dosage of 25 mg clozapine was sufficient to achieve normalized sleep architecture, remission of the depressive symptomatology, and normalization of NPT. It is likely that marked sedation is the mode of action of clozapine.

Administration, Oral↗
PubMed1989

Effects of trimipramine on sleep EEG, penile tumescence and nocturnal hormonal secretion. A long-term study in 3 normal controls.

Sleep EEG, nocturnal penile tumescence (NPT) and nocturnal endocrine activity were studied in 3 male control subjects during placebo, under trimipramine (TR) and after withdrawal. TR did not change the sleep structure. NPT activity tended to increase under TR. Nocturnal plasma cortisol levels decreased markedly while the early morning rise of cortisol appeared delayed under 200 mg TR. After withdrawal the changes of the cortisol secretion rebounded. Nocturnal secretion of GH, testosterone, LH and FSH remained unaffected, but plasma prolactin levels increased under TR and returned to normalcy after cessation. Our data illustrate that the neurobiological effects of TR are different from those of other antidepressants. We suggest that some of the psychotropic effects of TR are mediated by suppression of cortisol.

Adult↗
PubMed1989

Effects of fluoxetine upon pharmacoendocrine and sleep-EEG parameters in normal controls.

A single dose of 80 mg fluoxetine induced a slight increase in cortisol secretion when compared to placebo in an acute endocrine challenge test including assessment of prolactin, growth hormone, luteinizing hormone, follicle stimulating hormone, testosterone. This pretreatment with 80 mg fluoxetine did not change the ACTH release after blockade of the feed-back regulation of peripheral corticosteroids on ACTH secretion by metyrapone. Sleep-EEG revealed reduction of rapid-eye-movement sleep. Nocturnal penile tumescence activity was unaltered.

Adrenocorticotropic Hormone↗
PubMed1989

[Animal welfare legislation and animal experiments in Switzerland--effects and challenges].

The Swiss animal welfare legislation, which restricts experiments on animals, entered into force in 1981. The discussions, the legal prescriptions, the official guidelines and the ethical principles for animal experimentation issued by scientists are treated. The legislation has slowly brought about positive effects. Animal experimentation shows for several reasons a remarkable decline in the last years. Research on alternative methods to animal experiments was substantially promoted. Further improvements in the field of animal experimentation are requested.

Animal Testing Alternatives↗
PubMed1988

Effects of intravenous corticotropin-releasing hormone upon sleep-related growth hormone surge and sleep EEG in man.

Corticotropin-releasing hormone (CRH) plays a key role in coordinating neuroendocrine, metabolic and behavioral responses in stress and affective disorders. To further investigate the effects of enhanced pituitary-adrenocortical activity upon sleep-related phenomena we administered four intravenous injections of 50 micrograms human (h)-CRH or saline to 11 normal males at 10 p.m., 11 p.m., 12 p.m. and 1 a.m. and measured plasma levels of cortisol and growth hormone (GH) as well as sleep EEG recordings throughout the night. Treatment with h-CRH resulted in a significant increase of mean (+/- SEM) cortisol secretion between 11 p.m. and 3 a.m. (h-CRH: 100.6 +/- 9.5 ng/ml; saline: 39.0 +/- 1.5 ng/ml; p less than 0.01). This initial cortisol increase after repeated h-CRH stimulations was followed by a period of attenuated plasma cortisol between 3 and 7 a.m. (h-CRH: 70.3 +/- 7.0 ng/ml; saline: 115.5 +/- 8.0 ng/ml; p less than 0.01). Cortisol surges after h-CRH were associated with a significant blunting of sleep-related GH release expressed as areas under concentration curves (h-CRH: 1.245 +/- 0.32 ng/ml/min.10(3); saline: 2.462 +/- 0.92 ng/ml/min.10(3), p less than 0.01). In addition to these hormonal effects, h-CRH induced a decrease of REM and slow wave sleep (stages III and IV) while the amount of more shallow sleep (stages I and II) increased. These effects upon sleep structure were more pronounced during the second part of the night.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effects of clomipramine on sleep EEG and nocturnal penile tumescence: a long-term study in a healthy man.

The effects of the tricyclic antidepressant clomipramine on sleep EEG and nocturnal penile tumescence (NPT) were investigated during a long-term study in a normal male control subject. During 21 consecutive days the subject received first placebo for 3 days, then stepwise increasing dosages of clomipramine for 10 days, and finally placebo after withdrawal for 8 days. Under clomipramine, rapid eye movement (REM) sleep was suppressed markedly; an REM rebound occurred after withdrawal. Awake and stages 1 and 2 increased while slow wave sleep was diminished under clomipramine. Those non-REM parameters returned to baseline values after drug cessation. NPT was reduced simultaneously with REM sleep under clomipramine 30 to 75 mg. Under this dosage range, full erections occurred during the later hours of sleep in association with the delayed REM periods. Clomipramine 100 mg prompted a further decrease of NPT, which exceeded the REM suppression. Most of the changes and NPT parameters depended significantly on the dosage and the plasma concentration of clomipramine. After withdrawal, NPT needed 6 days to normalize. Although NPT was disturbed distinctly, no erectile dysfunction, but a decrease of sexual interest and, once, a lack of ejaculation, were reported.

Adult↗
PubMed1987

Effects of brofaremine (CGP 11 305A), a short-acting, reversible, and selective inhibitor of MAO-A on sleep, nocturnal penile tumescence and nocturnal hormonal secretion in three healthy volunteers.

The effects of brofaremine (CGP 11 305A), a short-acting, reversible and selective inhibitor of MAO-A, on sleep, nocturnal penile tumescence (NPT) and hormonal secretion during the night were studied during a long-term trial. Three healthy males underwent sleep-EEG and NPT recordings during consecutive nights (1) under placebo, (2) under stepwise increasing dosages of brofaremine and (3) under placebo after withdrawal. Hormone profiles were sampled during selected nights to analyze the plasma concentration of cortisol, HGH, prolactin, testosterone, LH and FSH. REM sleep was suppressed markedly under 150 mg brofaremine, while stages 1 and 2 increased. In comparison to the effect of irreversible MAOIs the REM suppression was shorter and did not persist after withdrawal. A decrease of the plasma concentration of the drug coincided with a return of sleep variables to baseline values. A REM rebound occurred after withdrawal of brofaremine. REM sleep and NPT showed a dissociation; NPT variables did not follow the decrease of REM sleep. The effects of REM parameters are correlated with the dosage and the plasma concentration of the substance. Intraindividually, a decrease in secretion of HGH was observed throughout the trial. No marked changes were found in the other endocrinological variables.

Adult↗
PubMed1987

Results of an open clinical trial of brofaromine (CGP 11 305 A), a competitive, selective, and short-acting inhibitor of MAO-A in major endogenous depression.

In an open clinical trial the authors treated 18 hospitalized patients suffering from endogenous depression with brofaromine (CGP 11305A), a competitive, selective, and short-acting inhibitor of type A monoamine oxidase (MAO). Four patients were defined as good responders, as they had a final HAMD score of between 0 and 7 points. Four patients were judged as improved, with final HAMD scores of between 8 and 15 points, while the remaining eight patients failed to respond (final HAMD score greater than or equal to 16 points). The major observations were a beneficial influence on drive in most patients, while paranoid symptoms worsened markedly, rendering the substance contraindicated in psychotic depression. Brofaromine appears to be safe and well tolerated and largely free of side effects. As objectified by the tyramine pressor test, dietary restrictions during brofaromine treatment require less stringency than is the case with conventional MAO inhibitors. The specificity of brofaromine to inhibit deamination is limited to MAO-A, since no reduction in platelet MAO activity was measurable. Sleep EEG recordings in a subset of patients reveals that the amount of rapid eye movement (REM) sleep is significantly reduced during brofaromine treatment.

Adult↗
PubMed1987

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls.

Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 +/- 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

Adult↗
PubMed1987

Stimulation response to corticotropin-releasing hormone (CRH) in patients with depression, alcoholism and panic disorder.

Alterations in baseline and challenged pituitary-adrenocortical function constitute the most extensively studied abnormalities in affective disorders. The recent availability of corticotropin-releasing hormone (CRH) for clinical studies opened the possibility to further investigate pathophysiology underlying aberrant ACTH and cortisol secretion. When injected to depressives CRH induces a blunted ACTH but normal cortisol release. Similar response patterns were observed among patients with panic disorder and alcoholism. In these diseases, enhanced baseline pituitary adrenocortical activity appears to be driven by a CNS disturbance resulting in overactive CRH secreting neurons. In addition to these endocrine findings we observed among normal controls suppressed nocturnal slow-wave sleep and growth hormone surges during infusions of CRH. Our clinical investigations with CRH support that this neuropeptide is involved in mediation of several neuroendocrine and behavioral changes frequently observed in depressive syndromes.

Adrenocorticotropic Hormone↗