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Biomedical subjects

P H Gruen

Publications and source records attributed to P H Gruen.

13 recordsLinked to original sources
PubMed1982

Cortisol's effects on human mental functioning.

Popularization of the dexamethasone suppression test has focused attention on the relation between cortisol metabolism and mood and behavior. This article considers the biochemistry, physiology, and pharmacology of cortisol and cortisol-like substances. In addition, the effects of external stresses on cortisol metabolism and circadian rhythmicity of secretory patterns are reviewed. Finally, managing exogenous cortisol excess in a clinical setting is discussed.

Affect↗
PubMed1978

Prolactin responses to neuroleptics in normal and schizophrenic subjects.

The prolactin response to neuroleptics can serve as an index of dopamine blockade in humans. Plasma prolactin increments to single doses of chlorpromazine, and prolactin decrements to single doses of levodopa, were similar in normal and schizophrenic subjects. Antischizophrenic drugs of all chemical classes stimulated prolactin release,while chemically related drugs and other psychotropic agents ineffective in schizophrenia did not. The prolactin response to neuroleptic therapy occurred in all patients, and tolerance did not develop. Within subjects, prolactin responses were graded according to neuroleptic dose, but the upper limit of sensitivity of the response curve was achieved at doses below the therapeutic range. Relative prolactin-stimulating potency in humans of chlorpromazine, thioridazine, trifluoperazine, butaperazine, and haloperidol correlated well with their relative clinical potencies.

Chlorpromazine↗
PubMed1976

Neuroendocrine studies of depressive illness.

Interest in possible neuroendocrine disturbances in endogenous depression is prompted by two lines of evidence: (1) clinical features of the illness suggest hypothalamic dysfunction; (2) the brain neurotransmitters implicated in depression also regulate neuroendocrine function. Our research reveals a marked, sustained hypersecretion in cortisol in severe depressive illness, which is apparently unrelated to stress and sleep disturbance, and which is associated with a distortion of the 24-hour cortisol secretory pattern. The hypersecretion is manifested primarily in the late afternoon, evening, and early morning hours, when cortisol secretion is normally inhibited. Growth hormone responses to hypoglycemia (but not to L-dopa) are also significantly reduced in endogenous depression, even when factors of age and the menopause are controlled. Postmenopausal depressed women appear to secret significantly less LH than normal postmenopausal women. Since all of these hormonal abnormalities can be reproduced by depletion of brain noradrenalin, the findings provide support for the the hypothesis of reduced functional noradrenergic activity in certain forms of depression.

Aged↗
PubMed1975

Growth hormone responses to hypoglycemia in postmenopausal depressed women.

Human growth hormone (HGH) responses to insulin-induced hypoglycemia were measured in ten postmenopausal women suffering from primary unipolar depressive illness, and in ten age-matched normal postmenopausal women. The mean maximal HGH response in the depressed patients was 4.6 plus or minus 4.4 ng/ml, and in the normals 13.3 plus or minus 9.8 ng/ml (P less than .05). All of the normal subjects had clinically adequate HGH responses, in contrast to only four of the depressed patients (P less than .01). The blood glucose responses were virtually the same in the two groups. Since brain catecholamines play a major role in mediating HGH responses to hypoglycemia, the findings are consistent with the hypothesis of diminished functional catecholaminergic activity in the depressed patients.

Aged↗
PubMed1975

Human growth hormone response to levodopa. Relation to menopause, depression, and plasma dopa concentration.

After ingestion of 500 mg of levodopa, postmenopausal women had significantly diminished human growth hormone (HGH) responses (mean, 4.6 ng/ml), as compared with those of age-matched men (mean, 9.1 ng/ml; P smaller than .05). The differences between the groups were not related to plasma dopa concentrations. The HGH responses to levodopa of age-matched unipolar and bipolar depressed men, and of unipolar depressed postmenopausal women, did not differ significantly from their respective normal control groups. Depressive illness of these types does not appear to affect the HGH response to levodopa, once the effect of the menopause is taken into account.

Adult↗
PubMed1975

Thioridazine stimulates prolactin secretion in man.

Thioridazine, unlike most other effective antipsychotic drugs, appears to be only a weak dopamine antagonist in various regions of the brain. We decided to test, indirectly, thioridazine's effects on another brain dopaminergic system, the tuberoinfundibular tract, which regulates prolactin secretion by stimulating hypothalamic secretion of prolactin-inhibiting factor. Chlorpromazine and several other phenothiazines have been shown to stimulate prolactin secretion. Five healthy men ingested 50 mg of chlorpromazine concentrate on one occasion, and 50 mg of thioridazine concentrate on another. Both drugs noticeably stimulated prolactin secretion within two hours. It is concluded that thioridazine is a potent dopamine antagonist in the tuberoinfundibular system, and it is suggested that this system's regulation of prolactin secretion may provide a useful method for studying antipsychotic drug effects in man.

Administration, Oral↗
PubMedDate not supplied

Reduced plasma LH concentration in postmenopausal depressed women.

Mean plasma LH concentration in postmenopausal women suffering unipolar depressive illness was 33% less than that of normal postmenopausal women (P less than 0.05). Since LH secretion after menopause is probably noradrenergically regulated, the finding provides support for the hypothesis of a functional noradrenaline deficit in depression.

Aged↗