Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cortisol resistance to suppression by 0.5 mg of dexamethasone given at 11 p.m. was studied in 30 normal subjects, 17 to 78 years of age. Serum cortisol concentrations were determined by radioimmunoassay. A strong positive correlation was found between age and cortisol concentrations 9 hours after dexamethasone administration. The data suggest that aging, per se, might contribute to the increased cortisol resistance to suppression by dexamethasone reported in depression and dementia.
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PMID:Aging and cortisol resistance to suppression by dexamethasone: a positive correlation. 658 89

The in vitro effects of six anaesthesia-related drugs and five stress-related serum factors on monocyte-mediated cytolysis and thymidine uptake in mitogen-(PHA)-stimulated lymphocytes have been studied. Thiopentone depressed both the monocyte and lymphocyte function in a dose-dependent way. However, at thiopentone concentrations which may be present in the serum after a single intravenous anaesthesia induction dose, the monocyte depression was moderate and depression of the lymphocytes was not observed. The other drugs tested, fentanyl, morphine, pancuronium, diazepam and bupivacaine, did not alter the cellular functions significantly. Prostaglandin-E2 in concentrations of 10(-6) and 10(-7) M markedly depressed monocyte-mediated cytolysis. Cortisol, catecholamines and serotonin did not alter this function. However, a synergistic depressive effect of the combination of prostaglandin-E2 and cortisol was observed. The proliferative response of PHA-stimulated lymphocytes was depressed by cortisol in concentrations of 2200 nmol/l and 1100 nmol/1 Again, there was a marked synergistic effect of the combination of cortisol and prostaglandin-E2, while prostaglandin-E2 alone, catecholamines and serotonin did not influence the PHA-response. A possible explanation for the depression of monocyte-mediated cytolysis and lymphocyte-thymidine uptake during and after surgery under general anaesthesia may be the combined effect of endocrine and local stress factors.
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PMID:Depression of monocytes and lymphocytes by stress-related humoral factors and anaesthetic-related drugs. 658 5

The mean 24-hour plasma level of cortisol with plasma sampling every 20-30 minutes was determined in 32 normal women aged 12-73, 40 normal men aged 10-55, 21 depressed women aged 20-61, and 11 depressed men aged 22-66. The mean levels of cortisol were higher in the group of depressives compared with the controls. Cortisol levels showed a significant linear correlation with age in normal women but not in normal men. Both depressed women and men had a significant linear increase of cortisol levels with age. The finding that age substantially contributes to increased levels of cortisol calls for cautious interpretation of any data concerning that hormone when the variable of age is not adequately controlled. Furthermore, aging and depression may have some underlying mechanisms whose elucidation may contribute to the understanding of the pathophysiology of vulnerability to affective disorders.
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PMID:Effect of age and sex on cortisol secretion in depressives and normals. 659 61

The present survey highlights the rationale for the use of state-dependent biological markers as predictors of clinical course in depression. Cortisol plasma levels after dexamethasone provide such a tool to monitor clinical progress. Since dexamethasone-resistant cortisol gradually returns to normalcy before a complete clinical remission is seen this measure has a possible predictive potential. Moreover, reversion to abnormal dexamethasone responses is prognostically infaust. Though the dexamethasone test has some merits, technical factors (e.g. exclusion criteria, dexamethasone-kinetics) which invalidate test results deserve careful consideration in future studies. Cortisol hypersecretion is considered as a physiological readout of a central disinhibition. This hypothesis is tested applying corticotropin-releasing factor and corticotropin in normal and abnormal DST responders. The data support the validity of the concept which assumes an intact but overactive pituitary-adrenal axis in a depressed subpopulation. A thesis is submitted which places the variety of biological disturbances in depression between two extreme viewpoints. One view considers all biological disturbances as sequelae to one particular dysfunction, e.g. disinhibition of corticosteroid secretion. The opposite view considers the myriad of biological disturbances as a sign of general loss of order, i.e. increased entropy, the precipitating mechanism of which is unknown.
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PMID:Prediction of clinical course by dexamethasone suppression test (DST) response in depressed patients - physiological and clinical construct validity of the DST. 666 28

An intravenous (0.2 mg) and an oral (40 mg) TRH-test was performed on 21 depressed patients (4 psychogenous, 17 endogenous); TSH, HGH, HRr, Cortisol, T3, T4 and RT4 were measured. The test was redone after 3 weeks of antidepressive treatment. Using an oral stimulation, it looks like there would be a possibility to differentiate into different groups according to the severity of illness. It also seems that the oral stimulation is a possibility to get information on the beginning effectiveness of antidepressive treatment. The responsiveness to the oral stimulus returns earlier than the response to the i.v. stimulation. Roughly, one can also differentiate between endogenous and psychogenous depression with an oral TRH test.
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PMID:TSH, HGH, HPr, and cortisol response to TRH in depressed patients. 679 65

The relationship of cortisol in blood plasma with plasma calcium and phosphorus was studied from 3 days before to 2.5 days after calving in 12 dairy cows (third or more parity). Cows were in three groups: 1) paretic (displayed hypocalcemic and lateral recumbency), 2) nonparetic (plasma calcium at least 8.0 mg/100 ml), and 3) borderline (plasma calcium less than 8.0 mg/100 ml). Cortisol concentrations from 0 to 1.5 days postpartum reflected the state of calcium stress of the groups, paretic more than borderline and borderline more than nonparetic. Phosphorus was lower from 0 to 1 day postpartum in paretic cows. Calcium and phosphorus were negatively correlated (within cow) with cortisol (-.53, -.37). In experiments with goats, cortisol was released in response to hypocalcemia and displayed no activity in initiating an onset of hypocalcemia when given exogenously. Also, the observation that cortisol-treated goats responded less severely with calcium depression and recovered faster from induced hypocalcemia by ethylene glycol-bis (beta-amino-ethyl ester) N,N'-tetraacetic acid infusions suggests cortisol may aid the animal in recovering from hypocalcemia.
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PMID:Elevated plasma cortisol during induced and spontaneous hypocalcemia in ruminants. 681 10

Chromosomal aberrations resulting from the exposure of Chinese hamster lung fibroblast cells to 95% oxygen have been used to investigate the protective effect of three steroids. Hydrocortisone had little useful effect. However, dosage of both methylprednisolone and dexamethasone could be increased to a level at which damage by oxygen was reduced to 50% of nuclei compared with 90% damaged in cells unprotected by steroids. There was no appreciable impairment of cell growth. Concentrations of steroids required for this effect were respectively 100 and 10 mumol litre-1, which corresponds to the high dosage regimen currently used to protect the lungs against the effects of endotoxic shock, haemorrhage and other conditions. The steroids did not protect against the depression of cell growth caused by 95% oxygen.
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PMID:Protective effect of steroids on cultured cells damaged by high concentrations of oxygen. 742 27

This study investigated diurnal variations in the affective and endocrine response to opioid blockade in man and whether there were effects related either to the dose of naloxone or the time of day at which it was given. Normal male subjects were given an intravenous bolus of either 0.2 mg/kg (study 1) or 1 mg/kg naloxone (study 2) or control infusions at two time points (0900 or 1800 hours) in a single-blind crossover design. Before and following each infusion, mood was measured by the Profile of Mood States (POMS) and a visual analogue scale (VAS), and blood samples taken at 15-min intervals. Cortisol, LH ACTH and vasopressin (study 2 only) were measured. Blood pressure and heart rate were also monitored. The lower dose of naloxone had no effect on overall mood (POMS), though tension and confusion were increased in the afternoon. The VAS showed increased depression in the afternoon, and heightened tension, sleepiness and reduced ability to concentrate at both times of day. The higher dose increased overall dysphoria at both time points, though the tension and depression subscales were not altered. VAS depression and tension were increased, and there were changes in sleepiness. Subjective reports showed that 45% of the subjects correctly identified the drug treatment at the lower dose compared with 89% at the higher one. ACTH increased after both doses of naloxone irrespective of time of day. Cortisol was also raised by naloxone; the effect was greater in the afternoon for the lower dose, but not the higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of naloxone on diurnal rhythms in mood and endocrine function: a dose-response study in man. 785 19

Studies in normal human subjects and animals suggest that the neuropeptide growth hormone-releasing hormone (GHRH) is a common regulator of the sleep EEG and nocturnal hormone secretion. In healthy volunteers GHRH prompts an increase in the amount of slow wave sleep (SWS) and in growth hormone (GH) secretion and blunting of cortisol release. Inhibition of GHRH may contribute to sleep-endocrine aberrances during depression. We tested the effects of pulsatile application of 4 x 50 micrograms GHRH on the sleep EEG and simultaneously investigated nocturnal hormone secretion in 10 inpatients (four females, six males) with the acute episode of major depression. In contrast to the effects of placebo, GH secretion increased distinctly and rapid-eye-movement (REM) density decreased during the second half of night. No other significant changes in sleep-endocrine activity, including SWS, cortisol and ACTH secretion, could be observed. We assume that hypothalamic-pituitary-adrenocortical system activity and slow wave sleep are inert to the influence of GHRH during acute depression. Cortisol and ACTH remained unchanged even in a subsample of five younger (aged 19-28 years) patients. This observation is in contrast to our recent finding that cortisol secretion is blunted in young normal volunteers after GHRH. But on the other hand, GHRH is capable of stimulating GH and inducing a decrease in REM density in these subjects.
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PMID:Growth hormone-releasing hormone (GHRH)-induced effects on sleep EEG and nocturnal secretion of growth hormone, cortisol and ACTH in patients with major depression. 793 84

The authors studied differences in cortisol response to controllable and uncontrollable stress and its relationship to Seligman's theory of learned helplessness in hospitalized unipolar depressed patients (11 nontreated, acutely depressed; 11 treated patients) and 11 age and sex matched controls hospitalized for traumatic surgery. Control and lack of control were achieved by induction of success and failure in a simple number addition test and applied in balanced order on 2 consecutive days. Saliva cortisol samples were collected before and after the test. No group differences in baseline cortisol levels were observed. Cortisol increased after uncontrollable and decreased after controllable stress in control patients, whereas cortisol decreased after both conditions in the acutely depressed group and less so in the treated group, although they were as emotionally upset after failure as controls. Thus, the normally observed ability of the neuroendocrine system to discriminate between controllable and uncontrollable stress deteriorates with increasing severity of depression.
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PMID:Cortisol reaction in success and failure condition in endogenous depressed patients and controls. 847 22


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