Biomedical subjects

S H Medbak

Publications and source records attributed to S H Medbak.

3 recordsLinked to original sources

PubMed1999

The effect of naloxone on adrenocorticotropin and cortisol release: evidence for a reduced response in depression.

BACKGROUND: Endogenous opioid peptides inhibit the hypothalamic-pituitary-adrenal (HPA) axis by influencing the release of hypothalamic corticotropin releasing factors. This study examines whether increased activity of the HPA axis in major depression is associated with reduced opioid tone. METHODS: We measured the adrenocorticotropin (ACTH) and cortisol responses to an intravenous bolus of naloxone 0.125 microg/kg in 13 depressed outpatients and 13 healthy volunteers. RESULTS: The mean cortisol response was significantly reduced (P<0.05), and the ACTH response was also non-significantly reduced in the depressed subjects. CONCLUSIONS: These findings imply that the degree of inhibitory endogenous opioid tone is reduced in depression. Various mechanisms for the finding are discussed, including possible alteration in the function of alpha-adrenergic pathways. CLINICAL IMPLICATIONS: Reduced endogenous opioid tone may explain why some depressed individuals self-medicate with opiates, and depression is associated with opiate withdrawal. Opioid pathways may have a role in the mechanism of action of antidepressant drugs, and may be of relevance in the development of novel antidepressants. LIMITATIONS OF THE STUDY: The sample size was small, leading to a failure of the difference of the basal cortisol levels and also the delta ACTH between the groups to reach statistical significance.

Adrenocorticotropic Hormone↗

PubMed1995

Central 5-hydroxytryptaminergic function in irritable bowel syndrome.

BACKGROUND: Psychological factors may contribute to the aetiology and exacerbation of symptoms in irritable bowel syndrome (IBS), suggesting that the central nervous system may be an important site of dysfunction in IBS. Hormonal responses after a serotonergic challenge assess the functional integrity of central 5-hydroxytryptaminergic pathways and are diminished in depression. The aim of this study was to determine whether hormonal responses in IBS after a serotonergic challenge would be decreased, as in depression, or exaggerated, as have been reported in another functional gastrointestinal disorder, nonulcer dyspepsia. METHODS: Fourteen IBS patients, 16 healthy volunteers, and 9 patients with inflammatory bowel disease were given 30 mg d-fenfluramine, a selective stimulus to central 5-hydroxytryptaminergic pathways. RESULTS: Plasma prolactin and cortisol concentrations during the following 5 h increased to a similar extent in all three subject groups, despite increased levels of anxiety and depression (as scored on the Hospital Anxiety and Depression Scale and Beck Depression Inventory) in the IBS and inflammatory bowel disease patients compared with the healthy controls. Base-line cortisol concentration correlated with the magnitude of affective disorder. CONCLUSION: In contrast to the alterations of central 5-hydroxytryptamine receptor sensitivity seen in depression and non-ulcer dyspepsia, central 5-hydroxytryptaminergic pathways function normally in IBS.

Adult↗

PubMed1993

Plasma prolactin, adrenocorticotrophic hormone and cortisol after administration of d-fenfluramine or placebo to healthy subjects.

Hormonal responses following single doses of the racemic drug d,l-fenfluramine have been used as an index of central 5-hydroxytryptamine (5-HT) function. We wished to evaluate normal responses to d-fenfluramine, which is more specific at stimulating 5-HT pathways. Twelve healthy volunteers were given 30 mg oral d-fenfluramine and placebo in a randomized single-blind crossover design. Following d-fenfluramine there was a rise in plasma prolactin, but no ACTH response. Cortisol levels did not rise above baseline values, but d-fenfluramine diminished the circadian fall in cortisol output, and cortisol levels were slightly higher after d-fenfluramine than after placebo. Unlike d,l-fenfluramine, d-fenfluramine is not a potent stimulus for ACTH and cortisol release. Hormonal responses following d-fenfluramine provide a more accurate assessment of the functional integrity of central 5-HT activity.

Adolescent↗