VIP decelerates non-REM-REM cycles and modulates hormone secretion during sleep in men.

Centrally administered vasoactive intestinal polypeptide (VIP) promotes rapid eye movement (REM) sleep in rats, rabbits, and cats. We studied the effect of 4 x 10 micrograms VIP (expt 1, n = 7) and 4 x 50 micrograms VIP (expt 2, n = 10) administered hourly as intravenous boluses between 2200 and 0100 on sleep electroencephalogram and secretion of plasma adreno corticotropic hormone, cortisol, growth hormone, and prolactin in humans. In experiment 2, the sleep cycles were decelerated during the first three cycles because of increased duration of both REM and non-REM sleep periods, and there was a tendency to increased REM-to-non-REM ratios.

Panic attacks caused by temporal tumors: an exemplary new case and a review.

A patient is described with a ruptured temporal cavernous hemangioma clinically presenting with recurrent panic attacks mimicking panic disorder. The role of temporal lobe structures in the pathogenesis of anxiety spells is highlighted, reviewing the published cases of temporal tumors leading to panic attacks.

[The effect of sedation on pulmonary function].

Opioids, benzodiazepines and hypnotics all affect central respiratory drive, muscular activity of the oropharynx, thoracic wall and diaphragm, bronchomotor tone and pulmonary vascular resistance (PVR), and may thus influence respiratory function during sedation and weaning. Opioids and benzodiazepines will attenuate hypercapnic and hypoxic stimulation of the respiratory centres. Compromise of respiratory drive must also be anticipated with ketamine, in view of recent evidence contradicting earlier findings of central respiratory stimulation.

Possible role of atrial natriuretic hormone in pituitary-adrenocortical unresponsiveness in lactate-induced panic.

Objective: This study investigated whether lactate-induced panic attacks in patients with panic disorder would activate atrial natriuretic hormone, which could explain the missing ACTH and cortisol response found in this kind of experimentally induced panic.

Method: Sodium lactate and placebo infusions were administered to 10 patients with panic disorder and to 10 healthy comparison subjects, and the atrial natriuretic hormone responses of the two groups were compared.

Results: During lactate infusion both the seven patients who had panic attacks and the eight comparison subjects who did not responded with increased plasma concentrations of atrial natriuretic hormone, but the patients had more pronounced surges of the hormone.

Efficient reactivation of Xenopus erythrocyte nuclei in Xenopus egg extracts.

Rapid genome replication is one of the hallmarks of the frog embryonic cell cycle. We report here that complete reactivation of quiescent somatic cell nuclei in Xenopus egg extracts depends on prior restructuring of the nuclear substrate and prior preparation of cytoplasmic extract with the highest capacity to initiate and sustain DNA synthesis. Nuclei from mature erythrocytes swell, replicate their DNA efficiently, and enter mitosis in frozen/thawed extracts prepared from activated Xenopus eggs, provided the nuclei are first treated with trypsin, heparin, and an extract prepared from unactivated, meiotically arrested, eggs.

Circadian changes in the sensitivity of the corticotropin-releasing hormone-stimulated HPA system after arginine vasopressin and atrial natriuretic hormone in human male controls.

In order to investigate whether modulation of the effects of corticotropin-releasing hormone (CRH) by arginine vasopressin (AVP) and atrial natriuretic hormone (ANH) is sensitive to circadian fluctuations, 12 healthy male volunteers were administered 100 micrograms hCRH during 30 min infusion of placebo, 3 IU AVP, or 150 micrograms ANH, the experiment being carried out in the morning (0800h) or in the evening (1900h). Compared with placebo, AVP significantly amplified the CRH-induced adrenocorticotropin hormone (ACTH) surge both in the morning and in the evening, whereas it enhanced cortisol secretion only in the evening. In contrast, ANH significantly reduced the ACTH surge, but only in the evening, and it reduced the cortisol surge in the morning compared to the evening.

Atrial natriuretic hormone inhibits corticotropin-releasing hormone-induced prolactin release in man.

Atrial natriuretic hormone (ANH) is found in heart myocytes, and also in the CNS. The inhibitory action of ANH on the hypothalamic-pituitary-adrenocortical (HPA) system has been established by in vivo and in vitro experiments, and could be of considerable importance: whereas several synergists to corticotropin-releasing hormone (CRH), the key hormone of the HPA system, are characterized in the past, until now ANH seems to be the only peptide which counterbalances the effects of CRH at the pituitary. As well as at the corticotroph, CRH has a stimulatory influence upon the lactotroph in vivo, and like ACTH and corticosteroids prolactin (PRL) is released in response to physical and cognitive challenges.

The hypothalamic-pituitary-adrenocortical system and sleep in man.

This review article summarizes the major findings about the interactions of human sleep structure and the hypothalamo-pituitary-adrenocortical (HPA) system under physiological and pathophysiological conditions, including studies that probe the sleep effects of systemically administered HPA hormones. Human sleep is regulated by a concerted action of various signal compounds acting at sleep-generating neurons whose central organization is not yet fully understood. During nocturnal sleep the endocrine system is remarkably active, the longest established finding being that growth hormone (GH) release is associated with the initiation of sleep and that there is a steep morning rise of cortisol (Weitzman et al.

Steroid effects on central neurons and implications for psychiatric and neurological disorders.

Acute and chronic stress as well as a number of psychiatric and neurological disorders are accompanied by profound disturbances of the HPA system. These neuroendocrine alterations act back on the central nervous tissue mainly via corticosteroids-affecting glucocorticoid and mineralocorticoid receptors. The major conclusions drawn from studies probing these receptors in clinical investigations are: (1) In many such conditions central corticosteroid receptors are weakened in their capacity to curtail spontaneous and stress-elevated corticosteroid levels; (2) the combined DEX-CRH test is the best neuroendocrine tool currently available for identifying HPA abnormalities in psychiatric patients; (3) in depression the decreased corticosteroid receptor capacity in transient, and antidepressants act through reinstatement of GR and MR function probably resulting in reduced hypothalamic CRH and AVP production; (4) several neurological disorders such as MS and HIV infection are often accompanied by altered HPA function, which has therapeutic implications; and (5) various corticosteroids, their biosynthetic precursors and their metabolites have differentiable effects on the sleep EEG, which can be attributed to their mode of action; specifically, steroids such as pregnenolone and DHEA most likely are produced in glia cells and act in a paracrine fashion at neurons, thus modifying the sleep EEG in humans in a manner that suggests their potential as memory enhancers.

Sleep endocrine effects of antigluco- and antimineralocorticoids in healthy males.

In several mammalian species the responsiveness of brain neurons to corticosteroids is mediated by mineralo- (MR) and glucocorticoid (GR) receptors. These receptors play a key role not only in the endocrine adaptation to stress but also in corticosteroid-induced changes of behavior, including sleep. We further explored the specific physiological role of this binary receptor system in the human brain by studying electroencephalogram (EEG) sleep and changes in plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and growth hormone from 1800 to 0700 h in a series of investigations in healthy men pretreated the previous evening with the nonselective GR agonist dexamethasone (Dex) and then receiving at 1400 h either placebo, spironolactone (Spi), an MR antagonist, or mifepristone (Mif), a GR antagonist.

Effects of pulsatile cortisol infusion on sleep-EEG and nocturnal growth hormone release in healthy men.

This study investigates the short-term effects of pulsatile cortisol administrations upon sleep electroencephalogram (EEG) and spontaneous release of growth hormone (GH) in humans. Ten young healthy male volunteers received intravenous injections of either placebo or cortisol every 60 min between 17.00 hours and 06.

Endocrine characterization of the new dopamine autoreceptor agonist roxindole.

Roxindole (5-Hydroxy-3-(4-phenyl-1,2,3,6-tetrahydropyridil-(1)-butyl)-indol) is a newly developed compound with a high dopamine autoreceptor agonistic potency at D2 receptors. Evaluation of roxindole for clinical purposes in psychiatric patients revealed that the substance has contrary to expectation merely negligible antipsychotic but considerable antidepressive effects. Interestingly it is nearly devoid of any side effects.

Endotoxin- and corticotropin-releasing hormone-induced release of ACTH and cortisol. A comparative study in men.

The present study compares the effects of endotoxin, a key factor in gram-negative bacterial infection, and of corticotropin-releasing hormone (CRH) on ACTH and cortisol secretion in healthy male volunteers in a placebo-controlled design. Endotoxin (isolated from Salmonella abortus equi; 0.4 ng/kg body weight) induced a significantly delayed and prolonged increase of ACTH and cortisol secretion as compared to CRH (100 micrograms), supporting the hypothesis that different intermediate mechanisms are involved (baseline/peak: ACTHEndotoxin vs.

Influence of endotoxin on nocturnal sleep in humans.

Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.

Brofaromine in panic disorder: a pilot study with a new reversible inhibitor of monoamine oxidase-A.

The therapeutic efficacy of brofaromine--a new reversible and short acting MAO-A inhibitor--was evaluated in 14 inpatients with a panic disorder. In an open trial, the patients were treated with placebo during the first week and with 150 mg brofaromine per day during the following four weeks. In all patients a distinct improvement in both anxiety and depressive symptoms was observed under the active drug.

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.

Modeling the pharmacokinetics and pharmacodynamics of dexamethasone in depressed patients.

Changes in time course effected by cortisol suppression and the relationship of these changes to the plasma dexamethasone concentration of suppressor and non-suppressor patients are described in this report on a combined pharmacokinetic-pharmacodynamic model. Thirteen depressed patients (8 suppressors and 5 non-suppressors) received an intravenous dose (1.5 mg) of dexamethasone.

Antiglucocorticoid treatment disrupts endocrine cycle and nocturnal sleep pattern.

Mifepriston (RU 486) is a steroid antagonist which binds with high affinity to glucocorticoid receptors (GR), and also to progesterone receptors. The antiglucocorticoid action of Mifepriston in man has been demonstrated by blockade of the negative feedback action of endogenous cortisol and by antagonism of the effects of exogenously administered dexamethasone. In the present study Mifepriston was administered to a normal male volunteer at 14.

Atrial natriuretic factor inhibits the CRH-stimulated secretion of ACTH and cortisol in man.

Corticotrophic secretion of ACTH is stimulated by corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), and suppressed by glucocorticoids. In vitro and preclinical studies suggest that atrial natriuretic factor (ANF) may be a peptidergic inhibitor of pituitary-adrenocortical activity. The aim of this study was to elucidate a possible role of ANF as a modulator of ACTH release in humans.