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Biomedical subjects

R S Nathan

Publications and source records attributed to R S Nathan.

48 records · Page 3Linked to original sources
PubMed1981

Cortisol secretion and dexamethasone response in depression.

The authors administered 2 mg of dexamethasone at 11:00 p.m. to 37 unmedicated hospitalized endogenously depressed patients and assessed their plasma cortisol response at 4:00 and 11:00 p.m. the next day. In addition, on nondexamethasone days 26 of these patients had mean 24-hour plasma cortisol concentration determinations from samples taken at 30-min intervals and 32 had plasma determinations from a single sample taken at 4:00 and 11:00 p.m. Mean 24-hour plasma cortisol concentration was elevated in 50%; only 7 of the 26 were dexamethasone resistant, and 6 of these 7 were hypersecretors. The authors suggest that dexamethasone resistance reflects the abnormality of cortisol hypersecretion in depression and that the 2-mg dexamethasone suppression test is a highly specific but not very sensitive indicator of hypersecretion.

Adult↗
PubMed1981

Failure of dopaminergic blockade to affect prolactin, growth hormone, and cortisol responses to insulin-induced hypoglycemia in schizophrenics.

The PRL, GH, and cortisol responses to insulin tolerance tests (ITTs) were evaluated in 12 medically healthy schizophrenic patients during a drug-free period and after 1 and 6 weeks of treatment with penfluridol, a potent, long acting, dopamine-blocking neuroleptic. Hypoglycemic responses were the same before and during penfluridol therapy. Although resting PRL levels were evaluated during initial penfluridol therapy (week 1), hypoglycemia provoked a further substantial PRL increment, not significantly different in magnitude from that induced by hypoglycemia during the drug-free period. However, there was a 54% reduction (P less than 0.05) in the increase in the area under the PRL curve during week 6 compared to the drug-free period. Regarding GH and cortisol, resting levels, areas under the curve, and maximal increments after ITT were essentially the same during weeks 1 and 6 of penfluridol treatment as in the drug-free period. The failure of 1 week of dopaminergic blockade to significantly alter the hormonal (PRL, GH, and cortisol) responses to ITT in the group as a whole suggests that dopamine-blocking mechanisms play little role in mediating these responses, at least in schizophrenic patients.

Female↗
PubMed1980

Dextroamphetamine and cortisol in depression. Morning plasma cortisol levels suppressed.

Dextroamphetamine sulfate administered intravenously in the morning to 11 unmedicated depressed patients suppressed previously elevated plasma cortisol levels to normal in 90 minutes, a fall of 33% from baseline. Ten other depressed patients, without amphetamine, maintained high cortisol levels during the same time period. In each of five normal young men, amphetamine identically administered stimulated a rise in cortisol between 15 and 30 minutes after infusion, an acute response absent in ten of the 11 depressed patients; by 90 minutes after amphetamine administration, plasma cortisol had fallen to normal and identical levels in both groups. Since noradrenalin normally inhibits hypothalamic corticotropin releasing factor (and adrenocorticotropic hormone) secretion, a noradrenergic deficit may account for cortisol hypersecretion in depression; amphetamine may transiently "correct" this deficit in depressed patients, thereby reducing their cortisol secretion.

Adult↗
PubMed1980

The effect of benztropine mesylate on the prolactin response to haloperidol.

The interaction between cholinergic and dopaminergic systems in regulating prolactin responses was investigated in normal men by administration of haloperidol (0.5 mg IM), with and without benztropine (1.0 and 2.0 mg IM). The acute prolactin response (at 30, 45, and 60 min) to haloperidol plus benztropine was significantly delayed compared to the response to haloperidol alone, in the same subjects. However, between 90 and 120 min after drug administration, prolactin responses achieved were similar in the three drug conditions. The results suggest a modest cholinergic-dopaminergic antagonism in the tuberoinfundibular system, apparent at low doses of neuroleptic and high doses of anticholinergic drugs.

Adult↗
PubMed1980

Effect of cyproheptadine and atropine on the diurnal prolactin responses to insulin-induced hypoglycemia in normal men.

There is a diurnal variation in the PRL response to insulin-induced hypoglycemia in normal men, with a substantially larger response in the evening. This study investigated the possible serotonergic and cholinergic influences on these diurnal PRL responses. Morning and evening PRL responses to hypoglycemia were compared in the same five normal young men without drug pretreatment, after cyprohepatadine, and after atropine sulfate. Cyproheptadine had no effect on the basal PRL concentration or the PRL response to hypoglycemia in either the morning or evening. Atropine had no effect on basal PRL concentrations in the morning or evening or on the morning PRL response to hypoglycemia. However, the evening PRL response was significantly inhibited by atropine (P less than 0.02), with an abolition of the normal diurnal difference in response (P less than 0.001) to insulin-induced hypoglycemia. These data suggest the involvement of a cholinergic mechanism in regulation of diurnal PRL responses to hypoglycemia.

Atropine↗
PubMed1979

Dopaminergic factors in human prolactin regulation: a pituitary model for the study of a neuroendocrine system in man.

This study in normal male subjects further investigates the effects of dopaminergic-antidopaminergic interactions as manifested by the prolactin response to dopamine and neuroleptic drugs. Incremental doses of dopamine hydrochloride (4 microgram/min, 15 microgram/min, 60 microgram/min, 300 microgram/min) were infused at a constant rate over 90-120 min after a fixed dose of a neuroleptic drug (sufficient for about half of the maximal prolactin response) had been given IV. A dose of dopamine in the order of 15-60 microgram/min appeared to match the "loss" of endogenous dopaminergic inhibition due to the antidopaminergic effect of the neuroleptic drug. The lactotrophic cells of the pituitary gland are suggested to serve as a model in man for the study of some basic neurohormonal mechanisms.

Adult↗
PubMed1979

Tardive dyskinesia presenting as a psychosis.

Tardive dyskinesia (TD), a movement disorder secondary to neuroleptic medication, is frequently found in psychiatric patients. The authors review reasons why some patients with TD go undetected. In addition, they report on another clinical situation which led to TD going undiagnosed: two cases which developed TD, then incorporated their movement disorder into a delusional system. Their clinicians focused exclusively on their psychosis, missing the underlying neurological disorder. How commonly this occurs in clinical practice is unknown.

Antipsychotic Agents↗
PubMed1979

Diurnal variation in the response of plasma prolactin, cortisol, and growth hormone to insulin-induced hypoglycemia in normal men.

Plasma PRL, cortisol, and GH responses to a standard iv dose of regular insulin were studied during the morning and evening in seven normal young men. Hypoglycemia achieved during morning and evening in the same aubjects was equal. There was a substantially greater maximal increment in PRL in the evening compared to the morning (P less than 0.01). The peak levels of cortisol achieved in the morning and evening were equal, but the evening maximal increase was greater (P less than 0.05) because of the significantly lower evening basal cortisol level. Evening increases in GH were greater than in the morning in five subjects and were essentially the same in two subjects; for the group, the evening maximal increment in GH was significantly greater (p less than 0.05 after log transformation). Since serotonergic mechanisms appear to be involved in the PRL, GH, and cortisol responses to hypoglycemia, we suggest the possibility of a diurnal variation in hypothalamic serotonin activity which may partly mediate these differential diurnal hormonal responses to hypoglycemia (although other neurotransmitters may also be involved). The data on cortisol are discussed with regard to the reset hypothesis of feedback inhibition.

Circadian Rhythm↗