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Biomedical subjects

M Schmauss

Publications and source records attributed to M Schmauss.

42 records · Page 3Linked to original sources
PubMed1984

Postdexamethasone prolactin and cortisol: a biological state variable in depression.

In 70 inpatients with major depressive disorder postdexamethasone cortisol and prolactin, but not baseline cortisol and prolactin, was found to correlate significantly with various state variables of depression. Postdexamethasone prolactin appeared to be a more specific state variable of depression compared with postdexamethasone cortisol. While prolactin was decreased following dexamethasone in controls and nonendogenous depressed patients, in endogenous depressed patients prolactin was increased by 30%. Due to this inverse prolactin response to dexamethasone, the sensitivity of this test should be considerably increased by using a higher dexamethasone dosage. The DST failed to be a diagnostic marker for any subgroup of depression.

Adult↗
PubMed1984

The DST and its relationship to psychiatric diagnosis, symptoms and treatment outcome.

The dexamethasone suppression test (DST) was administered shortly after admission to 102 consecutive in-patients with a Hamilton depression score greater than or equal to 16. Post-dexamethasone cortisol exceeded 6 micrograms/dl in 16 cases, and levels correlated significantly with Hamilton scores; with the AMP syndromes 'hypochondria', 'apathy' and 'catatonia'; and with the IMPS 'retarded depressive' syndrome. The criterion of suppression/non-suppression did not distinguish significantly between diagnostic categories (RDC or ICD), nor between endogenous and neurotic depression. (Newcastle scale). Both base-line and post-dexamethasone cortisol levels were reduced by prior treatment with minor tranquillisers, but not by major tranquillisers or antidepressants. DST results cannot be used as straightforward indicators of prognosis.

Adolescent↗
PubMed1983

Clinical investigations into antidepressive mechanisms. I. Antihistaminic and cholinolytic effects: amitriptyline versus promethazine.

It is assumed that established antidepressants exert their clinical efficacy by potentiation or decrease of central noradrenergic and serotonergic neurotransmission. However, recent experimental work suggests that antihistaminic and/or cholinolytic effects may also be involved. This double-blind controlled study compared amitriptyline (catecholamine potentiating, antihistaminic, cholinolytic) with promethazine (antihistaminic, cholinolytic) in 50 severely depressed inpatients over a 30-day treatment period. Analysis of the Hamilton depression rating scale revealed significant clinical superiority of amitriptyline over promethazine in such major depressive symptoms as depressed mood, suicidal ideation, psychic anxiety, and sleep disturbances. No significant difference was evident as far as autonomous side effects were concerned. Similar results were found by analysis of the AMP rating system. It is concluded that antihistaminic or cholinolytic effects per se do not explain the antidepressants' efficacy. However, potentiation of noradrenergic neurotransmission by cholinolytic activity might be the major antidepressive mechanism.

Adult↗
PubMed1982

Inhibitory effect of phentolamine on diazepam-induced growth hormone secretion and lack of effect of diazepam on prolactin secretion in man.

Phentolamine, a postsynaptic noradrenergic (NA) receptor blocker, inhibits diazepam-induced growth hormone (GH) secretion in man. In order to study the effect of phentolamine on six healthy subjects with a diazepam (10 mg i.v.)-induced GH increase greater than 7.5 ng/ml, it was necessary to test 11 subjects. The six diazepam GH responders showed a significantly higher (p less than 0.01) GH stimulation after diazepam alone than after diazepam plus phentolamine (60 mg i.v.). The inhibitory effect of phentolamine suggests that NA alpha receptors are involved in the diazepam-induced GH increase. Prolactin secretion after administration of diazepam (10 mg i.v.) was only slightly elevated in comparison with placebo (i.v.), suggesting that diazepam does not have an agonistic effect on dopamine (DA) receptors.

Diazepam↗
PubMed1982

Comparison of growth hormone stimulation induced by desimipramine, diazepam and metaclazepam in man.

A comparison of the effect on growth hormone (GH) stimulation in men (n = 6) of desimipramine (DMI), a tricyclic antidepressant, and of the benzodiazepine derivatives diazepam and metaclazepam with that of a placebo, showed that only DMI caused a significant (p less than 0.01) GH stimulation. After DMI, all six subjects showed a GH stimulation greater than 7.5 ng/ml, whereas after diazepam or metaclazepam, only three of the six subjects showed GH stimulation greater than 7.5 ng/ml, and the other three showed only a very small change, or no change at all in GH secretion. Higher GH stimulation occurred after diazepam (10 mg i.v.) than after diazepam (10 mg p.o.). No dose-dependent difference in GH stimulation after metaclazepam (10 and 30 mg p.o.) was apparent. No side effects appeared after administration of DMI during the test period (180 min); however, after administration of the benzodiazepine derivatives, sedative effects were clearly noted. DMI thus causes reliable GH stimulation in healthy male subjects, whereas GH stimulation could only be measured in some of the subjects after diazepam and metaclazepam.

Adult↗