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Biomedical subjects

K Wiedemann

Publications and source records attributed to K Wiedemann.

At least 55 records · Page 3Linked to original sources
PubMed1997

Influence of clonidine on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide in patients with panic disorder.

The influence of clonidine pretreatment on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide (CCK-4) was characterized. Patients with panic disorder (DSM-III-R) were given 50 micrograms CCK-4 i.v. at 1100 hours on 2 separate study days. In a randomized double-blind design they were additionally infused with 150 micrograms clonidine or placebo from 1040 to 1110 hours. After CCK-4 all patients experienced symptom attacks. No effects of clonidine on panic psychopathology or blood gas parameters were observed. After CCK-4, in the clonidine condition the pituitary release of adrenocorticotropin (ACTH) and prolactin was seemingly enhanced compared to placebo. Our results suggest that CCK-4-induced panic attacks are not suppressible by presynaptic alpha-2 receptor stimulation. Moreover, they point to a synergistic postsynaptic action of clonidine to CCK-4 upon pituitary hormone secretion. The diverging sites of action might possibly explain the discrepancies of psychopathological alterations and stress hormone secretion.

Adrenergic alpha-Agonists↗
PubMed1997

[High frequency jet ventilation during tracheal resection in children and infants].

Between 1986 and 1996, 16 infants and children less than 11 years of age (m = 11, f = 5) underwent resections for acquired or congenital tracheobronchial stenoses. During this period, various techniques of total intravenous anaesthesia (TIVA) were employed (midazolam, fentanyl, pancuronium; propofol, fentanyl, pancuronium). During the phase of dividing the airways, high-frequency-jet ventilation (HFJV) into the trachea or the main bronchi by 8-12Fr catheter(s) was applied for 10-75 min with driving pressures between 0.3-1.8 bar, frequencies between 100-200/min, I:E ratio between 1:4-1:1, and FjetO2 1.0. Catheter position was controlled visually, gas exchange was monitored by pulse oximetry and blood gas analysis. There were two incidents of transient hypoxaemia (paO2 less than 60 mmHg), and 4 cases of hypercapnia (paCO2 more than 45 mmHg). No complications due to the HFJV-catheter technique, such as barotrauma or aspiration were seen. All children were kept postoperatively on a ventilator due to swelling of the airway anastomosis. In 5 children ventilator treatment exceeded 7 days, 3 children were discharged tracheostomised. These observations serve to confirm that HFJV is capable of maintaining gas exchange during tracheal resection in infants and children, if the following prerequisites are met: 1. Tracheobronchial pathology suitable for poststenotic placement of jet catheter. 2. No respiratory impairment by parenchymal pathology. 3. Monitoring by continuous visual control of respiratory mechanics, pulse oximetry and blood gas analysis. Cardiopulmonary bypass should be applied if airway pathology precludes safe placement of jet catheters, or in the presence of parenchymal respiratory failure.

Anesthesia, General↗
PubMed1997

Illumination perception in photophobic patients suffering from panic disorder with agoraphobia.

Ten (6.9%) of a sample of 144 patients with panic disorder and agoraphobia developed photophobic behaviour in the course of their anxiety disorder. Their illumination ratings were characterized before and after cognitive behaviour therapy and compared to 10 age- and sex-matched normal control subjects. The illumination of a sheet of printed paper by a continuously adjustable reading lamp was rated by the subjects as 'too dark', 'comfortable' or 'too bright'. The ratings for comfortable luminance were significantly lower in the photophobic patients than in the controls, and renormalized after cognitive behavioural therapy. No differences were observed in the ratings for 'too dark' and 'too bright'. Photophobia in a subsample of patients with panic disorder is a state-dependent phenomenon that can be influenced by cognitive behavioural therapy. The role of neurotransmitters, conditioning processes and a concomitant neurasthenic syndrome requires further characterization.

Adolescent↗
PubMed1997

Autonomic reactivity and hormonal secretion in lactate-induced panic attacks.

To compare autonomic and neuroendocrine responses during lactate-induced panic attacks, heart rate variability and cortisol and atrial natriuretic hormone (ANH) levels were measured in patients with panic attacks and in healthy control subjects. In a randomized double-blind design, all subjects received either 10 ml/kg body weight of 0.5 M racemic sodium lactate or normal saline from 1100 to 1120. Spectral analysis of the R-R interval of analog electrocardiograms was performed, and total (0.001-0.45 Hz), low-frequency (0.01-0.05 Hz), midfrequency (0.05-0.15 Hz), and high-frequency power (0.15-0.45 Hz) were computed. Cortisol was measured 12 times in the period from 0900 to 1300, and ANH was measured at 1100, 1120, and 1200 by radioimmunoassay. In both panickers (n = 6) and nonpanickers (n = 8), an infusion of lactate resulted in an acceleration of heart rate, a reduction in total spectral power, and a decrease in the high- and low-frequency components of spectral power. Panickers showed a significant enhancement of the high-frequency power, whereas in nonpanickers, a shift from the mid- and high-frequency toward the low-frequency power emerged. ANH plasma concentrations during lactate infusion in panickers showed a significant increase (115 and 131% at 1120 and 1200, respectively, over concentrations at 1100) in contrast to nonpanickers (20 and 74%, respectively). No group or treatment effects on cortisol secretion emerged, which is in line with former reports. Our study supports preliminary observations that lactate-induced panic attacks enhance the release of ANH, a vasodilatator and inhibitor of sympathetic activity. Hence this hormone not only could inhibit the secretion of the stress hormone cortisol but, in parallel, could also attenuate the sympathetic stimulation to the heart. These inhibitory effects of ANH could explain the so-far-unresolved dissociation between psychopathological alterations and autonomic and endocrine responses of panic attacks.

Adult↗
PubMed1997

Corticotropin-releasing hormone inhibits melatonin secretion in healthy volunteers--a potential link to low-melatonin syndrome in depression?

Interactions between the hypothalamic-pituitary-adrenocortical (HPA) system and melatonin secretion have been demonstrated, but only the effects of melatonin on the activity of the HPA system have been studied in man. Alterations of melatonin secretion described as low-melatonin syndrome have been demonstrated in patients suffering from a major depressive episode, and an inhibitory factor on melatonin secretion has been postulated. We investigated whether corticotropin-releasing hormone (CRH), which is thought to be involved in HPA abnormalities in depressed patients, can also suppress melatonin secretion in healthy volunteers. Ten healthy male human volunteers in a double-blind study design received randomized hourly intravenous injections from 08.00 to 18.00 h that contained 10 micrograms human CRH, 1 microgram adrenocorticotropic hormone (ACTH), or placebo to simulate pulsatile hormone secretion. Plasma melatonin and cortisol responses during the treatment and nocturnal sleep electroencephalograms after the treatment were recorded. Administration of CRH reduced melatonin secretion significantly below values obtained after administration of placebo and ACTH. Cortisol secretion was significantly enhanced by ACTH in comparison to both placebo and CRH. Electroencephalographic sleep parameters revealed no treatment effects. Our findings suggest that CRH has an inhibitory effect on the pineal secretion of melatonin in normal man. A mechanism via a release of cortisol was not supported by our results. Secondary hormonal effects from changes in nocturnal sleep architecture were excluded. Further investigation of the action of CRH on melatonin secretion as well as the mutual feedback between the HPA system and the pineal gland may extend our knowledge of neuroendocrine alterations mediating the adaptive response to stress and the eventual involvement in the pathogenesis of depression.

Adult↗
PubMed1997

Central and peripheral administration of atriopeptin is anxiolytic in rats.

The effects of the central and peripheral administration of atriopeptin II, a 23-amino acid residue peptide of atrial natriuretic peptide (Ser103-Arg125) on anxiety-related behavior and on locomotor activity, was studied in male Wistar rats. Their behavior on the elevated plus-maze after social defeat stress indicated that intracerebroventricular (2.5 and 5 micrograms) and intraperitoneal (50 micrograms) administration of atriopeptin II produced anxiolysis. A low dose of 0.25 micrograms atriopeptin II administered bilaterally into the central nucleus of the amygdala was also found to be anxiolytic. Because intracerebroventricular administration of 5 micrograms atriopeptin II did not affect locomotor activity in the open-field test, the possibility that the anxiolytic effect was secondary to sedation could be ruled out. The anxiolytic effects observed after central and peripheral administration support the idea that atrial natriuretic peptide, which is increased in panic-anxiety, may be involved in the tapering of anxiety-related behavior.

Adrenocorticotropic Hormone↗
PubMed1997

C-type natriuretic peptide exerts stimulatory effects on the corticotropin-releasing hormone-induced secretion of hormones in normal man.

C-type natriuretic peptide and atrial natriuretic peptide have been reported to bind to distinct receptors and to exert opposing effects on different systems. Although it is known that atrial natriuretic peptide inhibits the corticotropin-releasing hormone-stimulated hormone release in man, the corresponding action of C-type natriuretic peptide has so far not been characterized. We investigated the effects of 30-min infusions of 150 and 300 micrograms C-type natriuretic peptide on adrenocorticotropin, cortisol, and prolactin release stimulated by 100 micrograms corticotropin-releasing hormone and on cardiovascular parameters in 8 healthy male volunteers. Compared with placebo, 300 micrograms C-type natriuretic peptide significantly (P < 0.05) enhanced the stimulation of cortisol (area under curve (arbitrary units): 520 +/- 35 vs 651 +/- 55) and prolactin (area under curve: 29 +/- 3 vs 37 +/- 5). Adrenocorticotropin levels were increased, but the differences did not reach statistical significance (maximum increment: 27 +/- 4 vs 36 +/- 2 pg/ml). C-type natriuretic peptide at a dose of 150 micrograms had no clear effect on these hormones and C-type natriuretic peptide also produced no cardiovascular or subjective effects. Our data suggest stimulatory effects of C-type natriuretic peptide on corticotropin-releasing hormone-induced hormone release and offer further evidence for a complex role of different natriuretic peptides in endocrine regulation.

Adrenocorticotropic Hormone↗
PubMed1996

Flumazenil attenuates the pituitary response to CRH in healthy males.

Differential effects of flumazenil (an antagonist) and midazolam (an antagonist at the benzodiazepine receptor) were studied in 8 healthy males. Adrenocorticotropic hormone (ACTH) and cortisol responses to a corticotropin-releasing hormone (CRH) challenge were measured. ACTH response was significantly lower after flumazenil administration than after saline or midazolam. No significant treatment effect was found for the CRH-induced cortisol secretion. Our results agree with previous reports that point to an agonistic effect of flumazenil on pituitary-adrenocortical system activity and, moreover, may further support the anxiolytic activity of flumazenil in stimulated stress.

Adrenocorticotropic Hormone↗
PubMed1996

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. With a low VIP dose, prolactin levels were decreased during the whole night, whereas, with a high dose, they were increased during the first half of the night. In experiment 2, the cortisol nadir was advanced, after midnight the serum cortisol levels were enhanced, and the growth hormone peak was blunted. It appears that VIP may have a phase-advancing effect on sleep cycles and cortisol secretion, possibly through actions that involve the suprachiasmatic nucleus.

Adrenocorticotropic Hormone↗
PubMed1995

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. During ANH infusion plasma AVP levels were suppressed both in the morning and in the evening, pointing to a hypothalamic site of action in addition to the pituitary and adrenocortical effects. The ACTH secretion profiles were indistinguishable between morning and evening in all three experimental conditions, whereas cortisol profiles differed significantly depending on the time of day in the AVP and ANH condition, but not for placebo.

Adult↗
PubMed1995

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., 1966; Takahashi et al., 1968). Moreover, the effects of exogenously administered corticosteroids and of their excessive endogenous release (e.g. Cushing's disease) were recognized more than 20 years ago.

Adrenocorticotropic Hormone↗
PubMed1995

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. CONCLUSIONS: Because atrial natriuretic hormone suppresses both pituitary ACTH and adrenal cortisol release, the authors suggest that the immediate rise of atrial natriuretic hormone explains the reported lack of pituitary-adrenocortical activation during lactate-induced panic.

Adrenocorticotropic Hormone↗
PubMed1995

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. Optimal replicating extracts are prepared from large batches of unfertilized eggs that are synchronously activated into the cell cycle for 28 minutes (at 20 degrees C). Because the Xenopus cell cycle progresses so rapidly, extracts prepared just a few minutes before or after this time have substantially lower DNA synthetic capacities. At the optimal time and temperature, eggs have just reached the G1/S boundary of the first cell cycle. This fact was revealed by injecting and replicating an SV40 plasmid in intact unfertilized eggs as described previously. We estimate that under optimal conditions approximately 6.14 x 10(9) base pairs of DNA/per nucleus are synthesized in 30-40 minutes, a rate that rivals that observed in the zygotic nucleus. The findings reported here are one step in our long term effort to develop a new in vitro/in vivo approach to nuclear transplantation. Nuclear transplantation in amphibian embryos has been used to establish that the genomes of many types of differentiated somatic cells are pluripotent. But very few such nuclei have ever developed into advanced tadpoles or adult frogs, probably because somatic nuclei injected directly into activated eggs fail to reactivate quickly enough to avoid being damaged during first mitosis. We have already shown that unfertilized eggs can be injected prior to activation of the first cell cycle. Future experiments will reveal whether in vitro reactivated somatic cell nuclei transplanted into such eggs reliably reach advanced stages of development.

Animals↗
PubMed1995

[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. Coordinated muscular activity of the oropharynx is important for airway patency. Since this mechanism is impaired more by benzodiazepines than by ketamine the latter may be advantageous during weaning. Respiratory frequency and tidal volume are both diminished by opioids, benzodiazepines and propofol. The differential impact on intercostal and diaphragmatic muscle activity may prove important in COPD and emphysema. With ketamine spontaneous respiration is increased. Gas distribution and airway pressures are influenced by bronchomotor tone. Bronchodilator effects are well known to arise with ketamine, but have also been demonstrated with benzodiazepines, propofol and some opioids. PVR is a critical factor in respiratory insufficiency. An increase in PVR with ketamine has been found during spontaneous respiration. Since evidence for pulmonary vasodilation during controlled ventilation has been recorded in humans and in vitro experiments, sedation regimens applied in respiratory insufficiency can also include ketamine.

Analgesics↗
PubMed1994

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.

Adrenocorticotropic Hormone↗