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Biomedical subjects

H Beckmann

Publications and source records attributed to H Beckmann.

At least 163 records · Page 9Linked to original sources
PubMed1989

Blunted adrenocorticotropin but normal beta-endorphin release after human corticotropin-releasing hormone administration in depression.

Since the discovery of CRH in 1981, several investigators have reported abnormalities of the hypothalamic-pituitary-adrenal (HPA) system in response to direct stimulation of the corticotroph cells in patients with psychiatric disorders. To further explore HPA system integrity in major depressive disorders, 13 drug-free patients and normal subjects matched for age, sex, ovarian status, and body weight received 100 micrograms synthetic human CRH as an iv bolus dose. Compared to that in the normal subjects, in the depressed patients a significant attenuation of the net ACTH release after CRH administration (772 +/- 597 vs. 263 +/- 286 pmol/min.L; P less than 0.02) was observed, while beta-endorphin and cortisol responses did not differ significantly between the groups. The magnitudes of ACTH and cortisol release were negatively correlated in the patient group only (r = -0.67; P less than 0.01). Thus, the blunted ACTH response to CRH in depression might be related to hypercortisolemia, while the implications of the apparent dissociation of ACTH and beta-endorphin after CRH administration still remain unclear. Our data support the hypothesis that the hyperactivity of the HPA system in depression most likely is a consequence of CRH hypersecretion, the origin of which may be explained by abnormal central glucocorticoid receptor or neurotransmitter regulation.

Adrenocorticotropic Hormone↗
PubMed1989

Moclobemide and maprotiline in the treatment of inpatients with major depressive disorder.

A double-blind study with the substituted benzamide moclobemide, a novel reversible, short acting MAOI with predominant inhibition of MAO-A, and maprotiline, the most selective noradrenaline reuptake inhibitor available at present has been conducted in n = 40 severely depressed inpatients suffering from predominantly endogenous depressions. No significant differences between the two drugs were found using global HRSD, HAMA and self rating scales. Regarding the clinical profile moclobemide seemed to be more effective in retarded depressives, maprotiline was superior in alleviating depressive agitation and sleep disturbances. The latter symptoms were responsible for three cases of treatment withdrawal in the moclobemide group. No case of hypertensive crisis could be registered, though patients were not subject to food restrictions. Maximal concentrations of moclobemide in CSF were reached two hours after oral application, compared to tricyclic antidepressants a high CSF/plasma ratio could be detected.

Anthracenes↗
PubMed1988

Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain.

Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 225% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.

Aged↗
PubMed1988

Delta sleep-inducing peptide response to human corticotropin-releasing hormone (CRH) in major depressive disorder. Comparison with CRH-induced corticotropin and cortisol secretion.

Twenty-four subjects (12 patients with major depressive disorder and 12 controls matched for sex and age) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an iv bolus dose. Healthy subjects exhibited a slight, but sustained, increase of plasma delta sleep-inducing peptide (DSIP) concentrations, whereas a marked reduction of DSIP levels was found in depressives. Compared to controls, depressed patients showed a significant attenuation of corticotropin (ACTH) responses, whereas cortisol secretion in response to hCRH was normal. Basal DSIP and cortisol concentrations were highly correlated and were higher in depressives than in controls. Both were negatively correlated with the DSIP responses to hCRH. These findings are compatible with the hypothesis that hypothalamic-pituitary-adrenal (HPA) overactivity in the depressive state is primarily due to central hypersecretion of CRH and support the view of a modulatory function of DSIP in the complex regulatory mechanism of the HPA system and of its pathophysiological significance for aberrant HPA axis function in major depressive disorder.

Adrenocorticotropic Hormone↗
PubMed1988

Growth hormone (GH) responses to GH-releasing hormone in depression: correlation with GH release following clonidine.

Twenty subjects (10 patients with major depressive disorder and 10 controls matched for age, gender, and ovarian status) received 1 microgram/kg synthetic human growth hormone-releasing hormone (GHRH)-44 amide as an i.v. bolus dose. Compared to controls, depressed patients showed a significant attenuation of net growth hormone (GH) responses to GHRH associated with normal basal GH concentrations. The blunted GH responses occurred in the face of significantly higher somatomedin C (Sm-C) concentrations. Comparison of GH responses after GHRH with GH output following the alpha 2-agonist clonidine (CLON) revealed a significant positive correlation. The concordance between GH responses after specific challenges at different levels of the GHRH-GH-somatomedin axis indicates the integrity of the hypothalamic-pituitary-somatotropic system in depression and supports the view that altered GH secretory patterns in depression may primarily be due to a suprapituitary disturbance.

Adult↗
PubMed1988

Endocrine parameters and biogenic amines in relationship to psychopathology after cholinergic drug challenge (RS-86).

The centrally active muscarinic agonist RS-86 elicited a dose-dependent anergic-anhedonic syndrome in a double-blind dose-response study in one healthy volunteer. At 4 and 5 mg, RS-86 induced escape from cortisol suppression by dexamethasone parallel to an increase in prolactin. The time course, as well as the absence of increases in plasma epinephrine and growth hormone, suggests that the changes are not due to nonspecific stress. However, there was a slight increase in plasma norepinephrine, tentatively dependent on the dose of RS-86. In 12-hour urine samples the excretion of 3-methoxy-4-hydroxy-phenylglycol and homovanillic acid tended to decrease in a dose-dependent manner, with a subsequent increase during the following nights. No systematic changes occurred in plasma dopamine, serotonin, and cyclic adenosine monophosphate or in plasma and urinary 3,4-dihydroxyphenylacetic acid or urinary vanillylmandelic acid. The findings are discussed in terms of the cholinergic-adrenergic balance hypothesis of affective disorders and biochemical findings in major depression.

Adult↗
PubMed1988

Corticotropin and cortisol response to human CRH as a probe for HPA system integrity in major depressive disorder.

To explore the integrity of the hypothalamic-pituitary-adrenal (HPA) system in major depressive disorder, 12 patients and normal controls matched for sex, age, and body weight received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Compared to controls, depressed patients showed an elevation in baseline cortisol and a significant attenuation of net adrenocorticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. These abnormalities in HPA axis function and apparent discordances in the interrelationships of ACTH and cortisol baseline and net stimulation responses between depressed patients and normal controls indicate, at least in part, a derangement of the glucocorticoid-dependent negative feedback circuitry and support the hypothesis that HPA hyperactivity in depression involves neurotransmitter-mediated hypothalamic hypersecretion of CRH.

Adolescent↗
PubMed1988

Growth hormone (GH) and prolactin responses after GH-releasing hormone in major depressive disorder: relationship to somatomedin C levels and dexamethasone suppressibility of cortisol.

To explore the growth hormone-releasing hormone (GHRH)-GH-somatomedin axis in major depressive disorder, 12 patients and 12 normal controls matched to the patients on age, sex, ovarian status and body weight received synthetic human GHRH-44 amide (1 microgram/kg) as an intravenous bolus. Compared to controls, the depressed patients showed a reduction in baseline plasma GH and a significant attenuation of net plasma GH responses to GHRH. The blunted GH responses occurred along with significantly increased somatomedin C (Sm-C) concentrations. The impairment of GH responses to GHRH and the increased Sm-C concentrations in patients with depression could have resulted from episodic hypersecretion of GH during the daytime, indicating integrity of the negative feedback circuitry. Normal feedback regulation suggests that diurnal episodic hypersecretion of GH reflects an abnormality at or above the level of the hypothalamus, so that the GHRH-GH-somatomedin axis hyperactivity observed in certain patients with major depressive disorder may be due, at least in part, to hypersecretion of hypothalamic GHRH. Our failure to demonstrate a difference in plasma prolactin (PRL) responses to GHRH between controls and depressed patients indicates that GHRH is not a PRL releaser in patients with major depression and that the altered GH secretory dynamics may not be directly related to the altered circadian PRL secretion linked to depression.

Adult↗
PubMed1988

[The cholinergic-adrenergic equilibrium hypothesis of affective psychoses].

The biochemical effects of antidepressant drugs generated the hypothesis of disturbances in the noradrenergic system in the pathogenesis of affective disorders. However, interference with the cholinergic system also yields psychotropic sequelae. Central cholinomimetics revealed antimanic properties as opposed to antidepressant effects of anticholinergics. Therefore, in extension of the catecholamine hypothesis and again based on the paradigm of pharmacological isomorphism, a cholinergic-adrenergic balance hypothesis has been suggested for affective disorders. This postulates a cholinergic predominance relative to noradrenergic activity in depression and the converse in mania. Although there are indications of inverse behavioural effects of cholinergic as opposed to catecholaminergic stimulation in man and animal, there is only few evidence at the neurophysiological and biochemical level in favour of the net effects depending on such a balance. However, only the direct demonstration of a biochemical defect can prove the balance hypothesis. More probably, interindividually different defects must be expected. They need not necessarily involve the synaptic signal transduction directly. Strategies and findings which might demonstrate biochemical disturbances are presented and discussed.

Affective Disorders, Psychotic↗
PubMed1988

Reflection of central aminergic-cholinergic imbalance by peripheral enzymes in psychiatric disorders?

Disturbances of central catecholaminergic-cholinergic balances have been discussed as causing affective disorders and schizophrenia. Such imbalances might be due to abnormalities of the metabolizing enzymes, especially their activities relative to each other. With this in mind, the activities of platelet monoamine oxidase and plasma butyrylcholinesterase (pseudocholinesterase) were determined spectrophotometrically in 33 psychiatric patients and eight controls. No significant differences could be detected for the enzyme activities as such and their relationship as expressed by their ratios. Thus, these peripheral enzymes seem to be unlikely indicators of supposed central imbalances.

Adult↗
PubMed1988

Insulin-like growth factor I in depressed patients and controls.

To explore the role of the somatomedin-mediated long-loop negative feed-back mechanism in altered growth hormone (GH) secretory dynamics associated with depression, plasma IGF-I concentrations were measured in 34 patients with a major depressive episode and matched healthy subjects. Compared with controls, depressed patients exhibited significantly increased plasma IGF-I concentrations. In the patient group plasma IGF-I concentrations were positively correlated with the maximum post-dexamethasone plasma cortisol concentrations. Our data suggest that increased plasma IGF-I concentration may reflect diurnal GH hypersecretion, contribute to deficient GH responses to dynamic challenges, and indicate an interrelationship between the hypothalamic-pituitary-somatotropic (HPS) and -adrenocortical (HPA) system regulation in depression.

Adult↗
PubMed1988

The cholinergic agonist RS 86: a pharmacopsychological study.

The cholinergic-adrenergic balance hypothesis of affective disorders postulates noradrenergic over-activity and cholinergic hypoactivity in mania and the converse in depression. Some evidence for cholinergic contributions to mood regulation derives from the antimanic and depressiogenic activity of physostigmine and arecoline. However, both drugs have pharmacodynamic and pharmacokinetic disadvantages. Therefore, the orally active muscarinic agonist RS 86 was tested in a double-blind dose-response study for its psychotropic effects in one healthy volunteer. A dose-dependent anergic-anhedonic syndrome was identified in comparison to placebo. The study confirms the physostigmine syndrome to be mediated by muscarinic, possibly M1 receptors, and gives further support to the hypothesis of a cholinergic modulation of mood and behavior in man.

Affect↗
PubMed1988

[Studies of the reliability and validity of the German version of the Montgomery-Asberg Depression Rating Scale (MADRS)].

In both its original and German version, the Montgomery-Asberg Depression-Rating Scale (MADRS) has proved to be efficient and practical, and the level of its interrater reliability would appear to be satisfactorily high. With regard to the detection of changes occurring during the course of a depressive phase, this scale exhibits a degree of sensitivity that is comparable to that reported for the HAMD. The concurrent validity between the MADRS and the HAMD is higher over time (.94) than in cross-section (.85). Factor analyses have demonstrated that the MADRS is capable of recording more psychological symptoms of depression than the HAMD. Thus, the MADRS should be applied in combination with other rating scales. Contrary to the intentions of the devisers of this scale, it has been found that, significantly different assessments may result when the same patient is rated by various groups (psychiatrists, psychologists, students and psychiatric nurses). These differences are of practical relevance and are greatest for the first assessment. Clearly, the selection of the time of rating as well as the length of the time period to be included in the evaluation are of particular importance. Even though it has been emphasized that the operationalization of the MADRS is very good, it would appear that also special training in the use of this rating scale is necessary.

Adult↗