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)

In order to investigate the role of serotonergic mechanisms in depressive disorders, the fenfluramine challenge test was performed in 31 patients suffering from different types of depression. The strategy was to select a simple method (i.e., easier to perform than CSF studies for instance) to be applied to a wide range of patients, as close as possible to everyday cases in a clinical setting (i.e., not only to such severe or highly selected groups as is normally the case in biological research in psychiatry). The neuroendocrine test (which consisted of the measurement of variations in the secretion of prolactin, growth hormone and Cortisol after the administration of 60 mg dl-fenfluramine p. o.) did not correlate with symptoms of behavior patterns previously identified with a "serotonin deficit" (i. e., suicidal behavior or attempts, lowering of the control of impulses, sleep disturbances) but only with the severity of the diagnosis (in the DSM-III hierarchical scale) or with indexes of endogeneity (Newcastle scale). This fact could be explained by methodological artifacts (i. e., dlfenfluramine is not a clean probe, showing influence in the dopamine and noradrenaline metabolism; the absorption of fenfluramine was not controlled) or by the fact that the involvement of serotonin in affective disorders is not a selective, isolated dysfunction, but is integrated in more complex interrelationships. Nevertheless, our preliminary findings (even without the results of the comparison with a control group and the evaluation of a few more data and cases) do coincide with the absence of predictors or the lack of specific patterns of response of symptoms with new selective re-uptake blockers of serotonin antidepressants.
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PMID:The fenfluramine challenge test in the affective spectrum: a possible marker of endogeneity and severity. 328 85

The effect of hydrocortisone (hydrocortisone sodium succinate) on bovine lymphocyte blastogenesis in response to Staphylococcus aureus antigens and phytohemagglutinin was measured in vitro. Lymphocytes isolated from the blood of cows were treated for 6 to 8 days with physiologic hydrocortisone concentrations known to be inducible by environmental stress (10 ng/ml), acute clinical mastitis (25 ng/ml), or adrenocorticotropin treatment (45 ng/ml). All 3 concentrations of hydrocortisone caused a depression (P less than 0.01) in lymphocyte blastogenesis in response to phytohemagglutinin and S aureus antigen extract. Hydrocortisone concentrations as low as 10 pg/ml caused a depression in the lymphocyte blastogenic response to phytohemagglutinin. Marked variation existed among cows in the normal response of their nontreated lymphocytes and in the degree of depression of lymphocyte function after the in vitro treatment with hydrocortisone. Macrophage depletion experiments showed that the suppressive effect of hydrocortisone was not mediated by induction of suppressor macrophages. The data suggest that T-cell function was impaired directly by hydrocortisone treatment.
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PMID:In vitro depression of bovine lymphocyte function by treatment of cultured bovine lymphocytes with physiologic concentrations of hydrocortisone. 340 Sep 21

In 42 major depressive inpatients, we analyzed the relationship between dexamethasone suppression test (DST) results and Minnesota Multiphasic Personality Inventory (MMPI) scales. Cortisol levels following DST were positively correlated with the depression as well as the social introversion MMPI scale scores, and negatively correlated with the hypomania scale scores. DST nonsuppressor depressives (n = 15) exhibited significantly higher scores on the social introversion scale and significantly lower scores on the hypomania subscale than DST suppressors (n = 27). Moreover, stepwise discriminant analysis using the hypomania score was able to correctly classify 71% of the sample according to DST dichotomy, whereas the association of other scales did not significantly improve the classification. Therefore, these results support a relationship between DST and depressive/manic psychopathology rather than anxious psychopathology.
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PMID:Dexamethasone suppression test and MMPI scales. 358 78

The effect of oral contraceptive use and hospitalization stress on the results of the dexamethasone suppression test (DST) were assessed. This test, in which 1 mg dexamethasone is given at 11:00 p.m., and blood cortisol is analyzed the following day, is used as an indicator or major or endogenous depression, as opposed to situational depression, but specificity of the test remains in dispute. The test subjects were 15 normal volunteers, mostly staff, and 27 surgical patients, who were planning orthopedic surgery the following day. Of the 20 women, 7 took oral contraceptives, (Sequilar, Microgynon 50, Trigynon, Microgynon 30 and Diane). Cortisol was radioimmunoassayed at 4:00 p.m. in volunteers and at 8:00, 4:00 and 11:00 p.m. in hospital patients. Only 1 subject had a positive test (non-suppressor), a non oral contraceptive user, with a cut-off point of 50 mcg/L. The hospital patients' cortisol levels were slightly higher (n.s.). Pill users' cortisol levels were unchanged.
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PMID:Lack of effects of hospitalization and oral contraceptives on DST results in control subjects. 367 80

Measurements of a variety of parameters of biologically active cortisol indicate that a small number of patients with depressive illness have significantly elevated levels of unbound plasma cortisol. Abnormalities in corticosteroid binding globulin do not account for the hypercortisolemia, and elevated urinary levels of free cortisol confirm the data obtained for plasma free cortisol. Direct measurements of free cortisol suggest that the absence of physical effects of cortisol in patients with depression is related to the very mild elevation in plasma levels of free cortisol in these patients and that high levels are not sustained throughout the day as they are in patients with pathologic glucocorticoid excess. The apparent discrepancy between elevated total cortisol levels and the mild elevation of unbound plasma cortisol is best explained by the generous binding capacity of corticosteroid binding globulin. Total cortisol levels of greater than 25 micrograms/dl are necessary to saturate the binding sites of corticosteroid binding globulin. Only then can free cortisol be detected in plasma. Although these studies suggest that unbound plasma cortisol is elevated, whether these levels represent biologically active cortisol in other tissue sites as well, particularly the central nervous system, is still unclear. It is well accepted that discrete binding sites for cortisol and dexamethasone occur in hypothalamic and pituitary tissue, but the mechanism of glucocorticoid regulation of these binding sites has not been elucidated. Cortisol levels in cerebrospinal fluid correspond closely to plasma levels of unbound cortisol. Ruf and Steiner have shown that corticosteroid responsive neurons are present in the periventricular gray matter of the third ventricle, where other investigators have identified active ependymal transport mechanisms for cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma free cortisol in depressive illness--a review of findings and clinical implications. 384 50

Cortisol concentration was estimated by a competitive protein-binding method in the lumbar cerebrospinal fluid (CSF) of patients suffering from depression or from mania, and compared with the CSF cortisol concentration of neurological control patients not suffering from an affective disorder. There were no significant differences between the groups.
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PMID:Cortisol in the cerebrospinal fluid of patients suffering from affective disorders. 509 56

It is fairly widespread clinical practice to administer large doses of corticosteroids to patients in cases of shock; doses of hydrocortisone as high as 50 mg X kg-1 given intravenously have been proposed and used. Hydrocortisone, when administered in this way during surgery, has been implicated in interactions with neuromuscular blocking agents. In order to determine the type and mechanism of this interaction, the authors undertook further investigation. The effects of hydrocortisone were studied in two ways. Firstly, a constant 50% depression of the indirectly elicited twitch tension of the tibialis-anterior muscle was established in cats, using a constant intravenous infusion of either pancuronium (1.0 +/- 0.2 micrograms X kg-1 X min-1) or succinylcholine (3.6 +/- 0.8 micrograms X kg-1 X min-1). The effects of intravenous hydrocortisone then were studied on this block. Secondly, cats chronically were treated with 2 mg X kg-1 of intramuscular hydrocortisone three times a week for 1 month, and then dose-response curves were constructed for pancuronium or succinylcholine. Acute administration of intravenous hydrocortisone (1-15 mg X kg-1) alone had no affect on the twitch tension of either the tibialis-anterior or soleus muscles, however, the corticosteroid (7 and 15 mg X kg-1) did significantly (P less than 0.05) enhance the 50% depression of the indirectly elicited twitch tension of the tibialis-anterior muscle produced by the constant intravenous infusion of pancuronium. The soleus muscle was affected similarly (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of acute and chronic hydrocortisone treatment on neuromuscular blockade in the anesthetized cat. 608 96

The metabolic and hormonal responses to exhaustive short-term supramaximal exercise were studied in 10 male physical education students. The exercise task was a single bout of running on the treadmill at 22 km X h-1 and 7.5% slope. It was performed with single oral doses of 100 mg Bupranolol (non-selective beta-blockade), 100 mg Metoprolol (beta-1-selective blockade), and placebo. Arterialized capillary and venous blood were sampled until 30 min post exercise. Time to exhaustion was 52.0 +/- 2.6, 47.6 +/- 2.0, and 46.0 +/- 1.9 s in the control, Metroprolol, and Bupranolol experiments. At cessation of exercise, adrenaline and noradrenaline were grossly elevated in all three conditions. Lactate and glucose increased markedly, this being accompanied by increasing insulin in the control and Metoprolol, but not the Bupranolol trials. Glycerol increased moderately, while FFA were depressed. Growth hormone showed a delayed increase at 15 and 30 min post exercise. Cortisol was unaffected by exercise. beta-blockade reduced the increases of lactate, glucose, glycerol, insulin, and growth hormone, exaggerated the depression of FFA and had no effect on cortisol. The results demonstrate that the strong sympatho-adrenal response to exercise of this nature is a major determinant of the increase of glucose at cessation of exercise. The hyperglycemia in concert with beta-2-adrenergic stimulation leads to elevation of insulin. Furthermore, lipolysis is controlled by beta-adrenergic stimulation. The delayed increase of growth hormone seems to be triggered by the declining glucose level during recovery.
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PMID:Metabolic and hormonal responses to exhaustive supramaximal running with and without beta-adrenergic blockade. 614 64

Cortisol concentrations in CSF were measured by radioimmunoassay in healthy controls, depressed patients, patients who had attempted suicide but were not depressed, and obsessive-compulsive patients. The factors that contributed most to the variance in CSF cortisol levels were a diagnosis of depression, height, and important life changes during the six months preceding the investigation. Depression was by far the most important factor. The depressed patients had significantly higher CSF cortisol levels than the controls. In obsessive-compulsive and depressed patients treated with clomipramine hydrochloride, the levels were significantly correlated with mean urinary cortisol excretion. Of the three monoamine metabolites measured, only 5-hydroxy-indoleacetic acid level was weakly correlated with CSF cortisol level. This correlation was confined to the depressed patients and could be accounted for by the common correlation with height.
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PMID:Cortisol in the CSF of depressed and suicidal patients. 615 64

Hydrocortisone (10(-4)M) causes a significant depression of cholic acid accumulation by the isolated rabbit ciliary body-iris while causing little, if any, depression of p-aminohippuric acid uptake and not affecting alpha-aminoisobutyric acid uptake. Because no lag period is present for this inhibition and because cyclohexamide pretreatments fails to eliminate it, the hydrocortisone effect does not appear to be mediated by a protein synthesis mechanism. Deoxycorticosterone (10(-4)M) not only inhibits cholic acid uptake but also depresses p-aminohippuric acid uptake; no deoxycorticosterone effect on alpha-aminoisobutyric acid uptake is seen.
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PMID:Steroid effects on uveal transport. 651 72


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