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)

Clinical measurements were made of the effects of various drugs on the stimulation threshold of human heart [right ventricle]. Of antiarrhythmic drugs, a marked and prolonged elevation of the stimulation threshold was produced by procainamide, quinidine, and aimaline. Relatively short-lasting elevation was elicited by local anaesthetics [trimecaine, lidocaine]. Beta-blockers were little effective. No detectable effect on the stimulation threshold was produced by phenytoin and digitalis glucosides from the group of antiarrhythmics. The deepest and most prolonged depression of the stimulation threshold was achieved with anabolics [nandrolone phenylpropionate, nandrolone decanoate] and with high doses of prednisone and of 6-methylprednisolone sodium succinate. Hydrocortisone was ineffective. A slight and brief depression was produced by atrophine. The effects of sympathomimetics were complicated: at stimulation with short pulses the threshold was always raised. At stimulation with long pulses the effects were variable, mostly biphasic [occasionally triphasic]: a transitory depression of the stimulation threshold was followed by a marked elevation. The I-t curve's slope altered. In exit block, sympathomimetics are indicated because of their chronotropic effect, not because of their questionable effect on the stimulation threshold. A number of drugs, often administered to stimulated patients, produced no effect on the stimulation threshold: antibiotics, nitrites, purine compounds, opiates, and others.
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PMID:Effect of drugs on the stimulation threshold of the human heart. 2 97

15 patients with formerly endogenous recurrent depression or manic-depressive illness free of psychotic symptoms, who are under lithium prophylaxis about 3,9 years, and 16 healthy controls with approximately the same age and sex were tested with 0,1 U Insulin/kg, 200 micrograms TRH and 50 micrograms LHRH for their hGH-, TSH-, hPRL-, FSH-, LH-and Cortisol levels about 2 hours. hPRL, FSH and LH did not show any change under lithium salts. All patients under lithium showed elevated TSH-levels under basal conditions and after stimulation compared with the control groups. For the young women before menopause the difference was highly significant. Men and praemenopausal women had significantly higher hGH-levels after stimulation under lithium than the normal controls. However postmenopausal women did not show this lithium effect on their hGH levels.
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PMID:[Neuroendocrinological changes under longterm therapy with lithium salts (author's transl)]. 11 22

Although the pigment leakage method is one of the most conventional for determining vascular permeability, accuracy in macroscopic measurement of the diameter of the stained area with an arbitary scale leaves much to be desired. We developed a simple and beneficial method for quantitative assay using a densitometer (Chromatoscanner CS-900). Guinea pigs weighing 300 approximately 350 g were used. Formalin as a phlogistic, in a dose of 2.3 approximately 37 mg was injected intradermally in the shaved skin of the back, and 15 mg/kg of pontamine blue was then given into the femoral vein. One hour after the injection the animals were sacrificed and the skin of the back, which was stained by the leaked pigment, was stripped off and allowed to adhere to a wooden plate for 24 hours. Reflection and a zig-zag scanning technique were used to measure the volume of the leaked pigment. There was a liner relationship between the dose of formalin and the integrated values. A dose-dependent relationship was also obtained when histamine, serotonin, kallikrein and bradykinin were used as phlogistics. Representative anti-inflammatory drugs such as aspirin, hydrocortisone, oxyphenbutazone, benzydamine, diclofenac sodium, sodium salicylate and aminopyrine depressed the leakage due to formalin. Depression of leakage by aspirin in a dose of 400 mg/kg was the most remarkable. Pigment leakage elicited by histamine, serotonin, kallikrein and bradykinin was examined on the same individual animal. Aspirin more than the other agents depressed the leakages due to bradykinin and kallikrein. Hydrocortisone and oxyphenbutazone depressed the leakage due to bradykinin, serotonin and histamine, but enhanced that due to kallikrein. The results obtained were consistent with those of a previous study and as this method is simple and more reliable, it is applicable for assay of anti-inflammatory compounds.
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PMID:[A new method for assaying anti-inflammatory drugs. Quantitative analysis of pigment leakage into skin by Chromatoscanner CS-900 (author's transl)]. 56 14

The proliferative response of rat peripheral blood lymphocytes and spleen cells to phytohaemagglutinin (PHA) was studied following treatment with single or multiple doses of hydrocortisone. A transient lymphopaenia with a rapid recovery at 24 h occurred with both dose schedules. Hydrocortisone in vitro caused a dose-dependent depression of blood lymphocyte response to PHA but enhanced the response of spleen cells when the steroid was added after the mitogen. An inverse relationship between blood and splenic lymphocyte responses to PHA occurred after a single dose of hydrocortisone. Blood lymphocytes from multiple dose hydrocortisone-treated rats had an enhanced response to PHA. Serum collected within 5 min of injection from single dose-treated rats depressed normal rat blood lymphocyte responses. After multiple doses of hydrocortisone serum enhanced blood lymphocyte responses to PHA. The primary antibody response to sheep erythrocytes was only affected by near toxic doses of hydrocortisone.
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PMID:Effect of hydrocortisone on the response of rat lymphocytes to phytohaemagglutinin. 70 21

A method of hard phasic separation of free and bound forms of the hormone demonstrated the presence of specific (saturated) and nonspecific (unsaturated) binding of dexamethazone in the cytosol of various rat organs; and increase of the sorbent concentration promoted a better detection of the first type of binding on account of selective depression of binding of the second type. Cortisol was bound with dexamethazone receptors of various rat organs in the binding sites common with dexamethazone, replacing the latter from its complex with the receptors. The constant of dexamethazone association with its receptors in the brain, liver lungs, spleen, thymus, and kidney cytosol was of the order of 10(8) M-1, with the binding capacity of cytosol of these organs within the range of from 0.6 to 4 ng hormone per 1 g of raw weight.
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PMID:[Study of the glucocorticoid receptors of the cytosol in various organs of the rat]. 88 38

The effects of oral prednisone on plasma and red blood cell cholinesterases have been studied in human volunteers. While the activity of plasma pseudocholinesterase is depressed by glucocorticoid administration, the activity of red blood cell true cholinesterase is not affected. Cortisol administration to rats, intraperitoneal or subcutaneous, inhibited liver pseudocholinesterase activity, indicating a possible depression of the enzyme protein synthesis.
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PMID:Effect of glucocorticoids on liver and blood cholinesterases. 92 92

Events preceeding the cortisol inhibition of uridine utilization by corticoid-sensitive P1798 lymphocytes have been investigated. When tumor cells were incubated with 1 muM cortisol for 15 min and then washed free of steroid and reincubated in the absence of hormone, the expected decrease of uridine uptake failed to appear 1.5 hr later. In contrast, the removal of cortisol after 30 or 60 min did not prevent subsequent development of the steroid effect. Addition of actinomycin D with cortisol, or 15 min after hormone treatment was started, blocked steroid action. However, when actinomycin D was added 30 or 60 min after the initial exposure to cortisol, hormone-induced depression of uridine uptake was no longer prevented. To study the role of protein synthesis, cycloheximide was added to the tumor cell suspensions at various times after cortisol treatment was started. Cortisol suppression of uridine utilization was blocked when cycloheximide was added with the hormone or 30 min after the start of hormone treatment. Cycloheximide added together with cortisol and washed out with the steroid after 30 min did not prevent subsequent appearance of decreased nucleoside uptake. Hydroxyurea, an inhibitor of DNA synthesis, did not prevent cortisol action, even when present throughout a 2 hr exposure to the steroid. Hormone removal or actinomycin D addition after 1.5 to 2 hr (when uridine uptake was already inhibited about 25%) did not prevent intensification of the steroid effect during a subsequent 1.5- to 2-hr incubation period, while addition of cycloheximide at this time completely prevented its progression. These results suggest aht: (a) cortisol inhibition of uridine uptake by P1798 lymphocytes involves an early irreversible step and appears to require continuing RNA but not protein synthesis during the first 15 to 30 min of hormone action; (b) protein synthesis but not RNA synthesis is required between 30 and 60 min; and (c) continuing protein synthesis but not RNA synthesis or hormone presence is necessary for the preestablished cortisol effect to progress.
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PMID:Sequential irreversible, actinomycin D-sensitive, and cycloheximide-sensitive steps prior to cortisol inhibition of uridine utilization by P1798 tumor lymphocytes. 114 29

This study examined hypothalamic-pituitary-adrenal axis functioning in a group (n = 25) of very carefully screened normal children with considerable attention to issues of adaptation and procedural stress. The subjects (mean age 10.3 +/- 1.6 y) were selected as "supernormal" controls as a part of a large psychobiologic study of childhood depression. After careful acclimatization over 24 h, the subjects underwent all-night sampling of plasma cortisol every 20 min, then the following evening had a corticotropin releasing hormone (CRH) stimulation test (using human CRH). Human CRH resulted in a rapid stimulation of adrenocorticotropin and cortisol. Adrenocorticotropin levels increased from 6.8 +/- 3.5 (+/- SD) pmol/L (30.7 +/- 16.1 pg/dL) to a peak of 11.6 +/- 5.5 pmol/L (52.9 +/- 24.8 pg/mL) at 15 min with return to baseline levels by 60 min. Cortisol levels increased from 131.4 +/- 59.7 nmol/L (4.8 +/- 2.2 micrograms/dL) to a peak of 427.0 +/- 113.5 nmol/L (15.5 +/- 4.1 micrograms/dL) at 30 min with return to baseline by 120 min. The cortisol peak was significantly greater (p less than 0.05) in boys [474.6 +/- 129.7 nmol/L (17.2 +/- 4.7 micrograms/dL)] than in girls [366.9 +/- 52.4 nmol/L (13.3 +/- 1.9 micrograms/dL, p less than 0.05)]. Age, body mass index, and pubertal status were not significantly related to hypothalmic-pituitary-adrenal axis measures. Nocturnal cortisol reached a nadir at 160 +/- 60 min after sleep onset (0102 h) and a peak 480 +/- 60 min after sleep onset (0612 h). Nocturnal cortisol levels were significantly (positively) correlated with human CRH-stimulated cortisol (r = 0.56, p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin releasing hormone stimulation test and nocturnal cortisol levels in normal children. 132 74

Both natural and adaptive immune responses were shown to be strikingly decreased in initial blood samples from 34 spinal cord injury and stroke patients. NK-cell function decreased to 24.8% (mean) 2 weeks after spinal cord injury in previously healthy young adults whose control group revealed a mean NK-cell function of 48.7%. This was accompanied at 2 weeks by increased plasma ACTH (mean of 17.0 pg/ml from 17 patients compared to a mean of 11.2 pg/ml from 12 controls) and urine free cortisol levels (mean of 152.1 micrograms/24 h from 9 patients compared to 53.6 micrograms/24 h from 15 controls). T-cell function and/or activation decreased to below normal values within 3 months after injury as revealed by lymphocyte transformation that was 32.8% of normal at 3 months. T-cell activation diminished as shown by a mean IL-2 receptor level of 179.3 units/ml in patients compared to 328.2 units/ml in controls. Serial monitoring of NK- and T-cell function revealed that specific physical rehabilitation therapy over a period of 6 months after injury restored NK- and T-cell function to near normal levels in most patients. This improvement was accompanied by a parallel rise in the patient's functional independence measurement scores. Results suggest critical neuroendocrine-immune system interactions in the restoration of immune function. Cortisol levels reverted to normal after 6 months of rehabilitation. Limited data suggest that natural immune system depression, NK-cell function, persists in spinal cord injury patients not receiving rehabilitation therapy (mean NK-cell lysis of 10.3%; p < 0.01).
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PMID:Neuroendocrine-immune interactions associated with loss and restoration of immune system function in spinal cord injury and stroke patients. 133 Dec 72

The aims of this study were to determine whether the administration of cortisol has a significant effect on mood in patients with depression and whether the effects of cortisol on changes in plasma hormone concentrations are like those of synthetic corticosteroids. Twelve patients had major depression and one each had dysthymic disorder and a depressive adjustment disorder. Five were male and nine were female. All were in-patients. Eight normal subjects, two females and six males, were used as controls. Basal beta-endorphin concentrations were 2- to 3-fold higher in depressed patients than in control subjects, but there were no significant differences between the patient and control groups in the basal (pre-infusion) plasma concentrations of ACTH, cortisol, growth hormone or prolactin. Cortisol, but not saline infusion resulted in a significant improvement in self rated mood. Surprisingly, cortisol infusion at first increased plasma beta-endorphin concentrations. At later times after cortisol infusion, plasma beta-endorphin concentrations decreased as did the plasma concentrations of ACTH and growth hormone; prolactin levels were increased. These results show (i) that cortisol infusion raises mood significantly in major depression, (ii) that plasma beta-endorphin concentration is a potential marker of major depression (iii) that rather than blunting of corticosteroid effects, responses to cortisol may even be enhanced in depressive illness. The unexpected, initial increase in beta-endorphin stimulated by cortisol, suggests that the action of cortisol is not simply one of negative feedback inhibition, but may involve mineralocorticoid, as well as glucocorticoid receptors.
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PMID:The effects of cortisol infusion upon hormone secretion from the anterior pituitary and subjective mood in depressive illness and in controls. 133 93


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