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Biomedical subjects

M Kellner

Publications and source records attributed to M Kellner.

At least 37 records · Page 2Linked to original sources
PubMed1998

Effect of flumazenil in lactate-sensitive patients with panic disorder.

OBJECTIVE: Flumazenil is a benzodiazepine receptor antagonist that has been reported to provoke panic attacks in patients with panic disorder. This study was undertaken to compare the effects of flumazenil and sodium lactate, the most widely studied panic provocation agent. METHOD: Ten patients with panic disorder were given infusions of saline, sodium lactate, and flumazenil in randomized order. Panic attacks, psychopathological changes, heart rate, and cortisol and ACTH secretion were recorded. RESULTS: Eight of the 10 patients experienced a panic attack after sodium lactate, but none did after flumazenil or saline. Cortisol and ACTH secretion were not enhanced by any of the treatments. Sodium lactate increased heart rate, whereas flumazenil had the opposite effect. CONCLUSIONS: These findings do not lend support to the view that the benzodiazepine receptors of lactate-susceptible patients with panic disorder are hypersensitive and that flumazenil can therefore act as an inverse agonist.

Adrenocorticotropic Hormone↗
PubMed1997

Tender points, depressive and functional symptoms: comparison between fibromyalgia and major depression.

The degree of symptomatic overlap between fibromyalgia and major depression should be estimated by assessing the amount of local tenderness and the frequency and severity of depressive and functional symptoms. Tender points were assessed by palpation and symptoms by psychometric scales in 30 patients with fibromyalgia and 26 patients with major depression. The patients with fibromyalgia had markedly more tender points (16.5) than the depressive patients (1.3). In contrast, depressive and functional symptoms were present in both groups of patients, and some depressive patients (26%) also suffered from clinical pain. An increased sensitivity to pressure pain clearly distinguishes fibromyalgia from depression even if there is an overlap of other symptoms.

Adult↗
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

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

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

[Initial experiences with dilatation of dialysis shunts with color-coded duplex ultrasonography monitoring].

PURPOSE: Aim of the study was to evaluate the technical aspects of colour coded duplex sonography guided interventions of peripheral vessels. METHODS: During 15 months 39 stenoses of shunt veins in 24 patients were dilated guided by colour coded duplex sonography. RESULTS: 38 stenoses were dilated without complications. The blood flow volume was increased from 361.9 +/- 83.5 to 718.9 +/- 189.2 ml/min. In one case it was not possible to dilate the stenosis because of a vasospasm. CONCLUSION: PTA guided by colour coded duplex sonography is an alternative to DSA guided interventions of superficial vessels without x-ray exposure or contrast agent application.

Adult↗
PubMed1996

[Coincidence of Pneumocystis carinii pneumonia and lung carcinoma in AIDS].

In a formerly drug-dependent patient of 35 years of age suffering from an advanced HIV infection there was a development within a period of a few months of rapid weight loss amounting to 12 kg, persistent subfebrile temperatures and progressive dyspnoea on exercise. The histological pattern obtained via bronchoscopy revealed not only pneumocystis carinii pneumonia, which had already been suspected clinically, but also a not very differentiated adenocarcinoma of the lung with lymphangiosis carcinomatosa. The patient died three months after tis diagnosis was established, which had been followed by the usual pneumocystosis therapy and palliative treatment with glucocorticoids.

AIDS-Related Opportunistic Infections↗
PubMed1995

Intermediate glucocorticoid feedback of corticotropin secretion in patients with major depression.

The effects of a 2-h infusion of a low dose of cortisol on concentrations of adrenocorticotropic hormone (ACTH) and cortisol were studied in six inpatients with recurrent major depression and six healthy volunteers. Each subject was studied twice and received, in random order, from 11:00 to 13:00 h a 25 ml/h infusion of either 3 mg/h of cortisol or saline. Blood samples for ACTH and cortisol determination were drawn between 10:45 and 13:00 h every 15 min. ACTH and cortisol measurements in patients did not differ significantly from those in volunteers at any of the time points tested. The finding of an intact intermediate feedback in depression, where nonsuppression on the dexamethasone suppression test is frequently observed, may be explained by the binding of cortisol at limbic and hypothalamic corticosteroid receptors, while dexamethasone acts primarily at the pituitary. Findings of this pilot investigation should be confirmed in larger groups of patients for whom data from the dexamethasone suppression test are also available.

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

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

Structure-activity relationships of phenyl- and benzoylpyrroles.

Antitumor, antimicrobial, and phytotoxic activities of the marine antibiotic pentabromopseudilin (1a) and related phenyl-, benzyl- and benzoyl pyrroles were compared. All activities depended strongly on the substituent pattern, with the natural compound 1a being the most active one. As judged from model reactions, a covalent bond of nucleophiles to the pyrrole system may be involved in the inhibition of macromolecular syntheses.

Animals↗
PubMed1994

[Neuropsychiatric symptoms in primary hyperparathyroidism].

Over a period of 3 months a 51-year-old woman developed a depressive syndrome with loss of memory, inability to find words, impaired fine movements and phases of spacial disorientation. Biochemical tests demonstrated occasional slight rises in serum calcium (2.8-2.9 mmol/l) and parathormone (4.6-5.2 pmol/l). She had a grade II nodular goitre with normal thyroid function. Ultrasonography of the thyroid suggested a right cranial parathyroid adenoma, confirmed at a right thyroidectomy with resection of the right upper parathyroid, while the other parathyroid glands were grossly normal. Calcium and parathormone levels returned to normal after the operation, as did the neuropsychiatric symptoms (within two months). This typical case illustrates that even in seemingly isolated neuropsychiatric changes an organic disease, like primary hyperparathyroidism, needs to be thought of.

Adenoma↗