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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous data from our laboratory have demonstrated that glucan administration significantly alters the course of a variety of experimentally induced infectious diseases. In view of the increasing incidence of gram-negative infections, studies were initiated to evaluate the effect of intraperitoneal glucan therapy on Escherichia coli-induced peritonitis and sepsis. Male ICR/Tex mice were injected intraperitoneally with glucan or dextrose on days 5 and 3 prior to intraperitoneal challenge with 1.0 x 10(8) E. coli. Glucan administration resulted in a significant enhancement of survival. Evaluation of the mechanism of protective action of glucan revealed that both the glucan and dextrose control groups showed an equivalent level of blood-borne E. coli at early periods. At 6 hours after challenge the glucan group showed a significant decrease in blood-borne E. coli. In contrast, the dextrose control group demonstrated progressive bacteremia. A significant depression of phagocytic activity occurred in E. coli-infected mice as compared with control mice that were not exposed to the bacterial challenge. The enhancement in phagocytic function observed in glucan-treated control mice was unaltered in E. coli challenged, glucan-treated mice. The possible importance of hyperfunctional macrophages in reduction of mortality from E. coli sepsis was denoted by methyl palmitate-induced reversal of the glucan hyperfunctional state. Methyl palmitate-treated glucan injected mice were not protected against E. coli infection. These data denote that the intraperitoneal administration of glucan significantly modifies the course of E. coli-induced peritonitis and bacteremia due, in part, to glucan-induced enhancement of macrophage function.
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PMID:Immunotherapeutic modification of Escherichia coli--induced experimental peritonitis and bacteremia by glucan. 633 16

Infections and chronic liver injury are common causes of morbidity and mortality in alcoholics, and both of these may be related to an altered immune response. This study describes a guinea pig model of chronic ethanolism designed to selectively study the cellular immune system in a setting free from the malnutrition, socioeconomic deprivation, and severe underlying hepatic dysfunction seen in human disease. Animals were given 2.5 g/kg/day of ethanol as a 15% solution in 0.9% NaCl or isocaloric-dextrose-saline control solution intraperitoneally in 2 divided doses for 5 weeks. At 2 weeks, the mean serum ethanol level 1 hr after treatment was 20.4 mM (range 8.9-30.6) while the mean serum acetaldehyde level was 55.1 microM (range 17.0-111). At 5 weeks the serum levels for ethanol and acetaldehyde were 20.1 mM (13.3-32.9) and 41.5 microM (2.4-87.6), respectively. Weight gain was persistent throughout the study and did not differ significantly between ethanol and control groups. After 5 weeks of treatment, lymphocyte response to the mitogens, phytohemagglutinin, and concanavalin A was significantly decreased in the ethanol treated group (p less than 0.05). Response to the specific antigen, picrylated human serum albumin, T & B cell per cent and number, skin test reactivity, peripheral white blood cell count, total lymphocyte count, and migration inhibitory factor production were not significantly altered by 5 weeks of ethanol treatment. Therefore, in a controlled animal model of chronic ethanolism, we observed a significant depression of lymphocyte blastogenic response which may, in part, explain the increased propensity to infection by intracellular pathogens seen in alcoholics.
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PMID:Ethanol-induced alterations in lymphocyte function in the guinea pig. 637 25

Intragastric pressures were recorded in bilaterally adrenalectomized male rats with insulin hypoglycaemia. A significant depression in intragastric pressure was noted following the administration of D-glucose injected into the hepatic portal vein but not after the administration of L-glucose, D-mannose, D-fructose, D-galactose, D-xylose or D-arabinose. The reduction in intragastric pressure induced by the portal administration of D-glucose was not reproduced following selective division of the hepatic branch of the vagus nerve. Of the three anomeric forms of D-glucose used (alpha-D-glucose, equilibrated D-glucose and beta-D-glucose), beta-D-glucose was most potent in reducing the intragastric pressure. These results suggest that the vagal afferents may convey information concerning glucose concentration in the portal vein to the central nervous system, and that the activation of such afferents may modulate gastric motility which is dependent on the anomeric stereospecificity of D-glucose.
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PMID:Inhibition of gastric motility induced by hepatic portal injections of D-glucose and its anomers. 637 52

Thirty-four patients undergoing elective abdominal aortic aneurysmectomy were studied, and they were randomly allocated to a "fed group receiving amino acid dextrose solutions intravenously and fat emulsions or an "unfed" group receiving standard postoperative care. Cell-mediated immunity was measured by lymphocyte count, the in vitro response to the T-cell mitogen PHA and determination of T-cell subsets using monoclonal antibodies. Serum suppressive activity was measured by the ability of the sera of the patient to suppress the response of normal lymphocytes to PHA. Feeding was continued for three to five days postoperatively until satisfactory oral intake was achieved. There was no significant improvement in lymphocyte count or blastogenesis postoperatively in the "fed" group, and operation did not lead to any alteration in the ratio of T-cell subsets, although there was a fall in T-cell count (OKT3 positive cells). We conclude that short term parenteral nutrition in well nourished patients, postoperatively, does not abrogate the depression of cell-mediated immunity which occurs after extensive operative procedures.
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PMID:The effect of short term postoperative intravenous feeding upon cell-mediated immunity and serum suppressive activity in well nourished patients. 642 72

Acute bracken fern toxicity in a calf was reproduced with ptaquiloside, a norsesquiterpene glucoside, isolated from the boiling water extract of bracken fern. Ptaquiloside was dissolved in 500 ml of saline and administered by drench at increasing dosages for six days out of every seven for the following periods: 400 mg/day for 24 days, 800 mg/day for 14 days and 1600 mg/day for four days. Neutrophilic granulocytes began to decrease markedly around 50 days after the start of the experiment, and granulocytopenia continued for a further 35 days until the autopsy, despite the discontinuance of ptaquiloside administration. Thrombocytes showed a relatively slow depression and reached 1 X 10(5)/mm3 at the lowest level. The calf was autopsied 86 days after the start of administration of ptaquiloside. Sternal bone marrow was found to be mostly replaced with fat marrow and only small foci of erythropoietic cells and a small number of megakaryocytes remained.
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PMID:Reproduction of acute bracken poisoning in a calf with ptaquiloside, a bracken constituent. 650 12

In a previous in vitro study we demonstrated reduced CO2 production in rat hippocampal tissue when metrizamide was added. This metabolic depression is believed to be a result of the 2-deoxy-D-glucose (2-DG) portion of the metrizamide molecule since 2-DG is a known competitive inhibitor of glucose metabolism. This competitive inhibition probably occurs at the cell membrane since it has never been shown that metrizamide penetrates neural cells. Further the inhibition is most likely related to competition for the membrane glucose carrier. A new nonionic contrast medium, iohexol, does not contain a 2-DG component and if the hypothesis for the metabolic inhibition is valid we should not expect metabolic inhibition with iohexol. This hypothesis was tested using the rat hippocampus model previously used for metrizamide. We compared iohexol with metrizamide in isotonic concentrations and also examined the effect of hypertonicity. These experiments did not demonstrate inhibition of CO2 production with iohexol at near physiologic osmolalities, however, there was a marked depressive effect with increasing osmolality. This effect from hypertonicity is, however, probably of less importance in vivo where water will rapidly diffuse toward the hypertonic areas. The apparent lack of interference of the iohexol molecule on glucose metabolism should therefore make iohexol a more suitable contrast medium, for subarachnoid investigations than metrizamide.
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PMID:The effect of iohexol on glucose metabolism compared with metrizamide. 651 Dec 66

Thirty healthy women in active labour received an intrathecal injection of morphine 0.5 mg (n = 12) or 1 mg (n = 18) in 7.5% dextrose. Both doses provided excellent analgesia for labour, 93% of patients obtaining at least 50% pain relief. Analgesia began 15-60 min after injection and did not decrease until 6-8 h after injection. Analgesia was satisfactory until distension of the perineum, either by forceps or the infant's head. The intrathecal injection of morphine did not adversely affect the condition of the infant. Eighty per cent of patients developed pruritus; 53%, nausea or vomiting, or both; 43%, urinary retention; and 43%, drowsiness. These side effects were decreased by naloxone, which did not affect the degree of analgesia. There was no significant depression of ventilation in any patient. These results suggest that morphine 0.5 mg or 1 mg, administered intrathecally, effectively decreases the pain of labour, and that i.v. administration of naloxone can alleviate the common side effects.
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PMID:Intrathecal administration of hyperbaric morphine for the relief of pain in labour. 654 39

Abnormalities in the oxidative metabolism of glucose in human cerebral gliomas have been studied in seven patients using positron emission tomography. Measurements of regional cerebral blood flow and oxygen consumption were obtained using the oxygen-15 steady-state inhalation technique. Values of regional cerebral glucose consumption were obtained using fluorine 18-labeled 2-fluoro-2-deoxy-D-glucose and a simplification of the method of Sokoloff. Functional values were obtained for regions of tumor and brain tissue in the middle cerebral artery territory of the contralateral cortex. Values of regional glucose consumption were calculated for both regions using a value of the lumped constant quoted for normal brain tissue (0.42). Tumor regional cerebral blood flow was comparable to that in the contralateral cortex, whereas regional cerebral oxygen consumption was depressed. This depression resulted in low tumor values of the fractional oxygen extraction ratio (0.21 +/- 0.07), indicating that oxygen supply exceeded the metabolic demand. In contrast, tumor regional cerebral glucose consumption was not depressed and regional glucose extraction ratios were similar for tumor and brain tissue. The metabolic uncoupling between regional oxygen consumption and regional glucose consumption (CMRO2/CMRGlu = 0.24 +/- 0.07 ml of oxygen per milligram of glucose) is indicative of increased aerobic glycolysis.
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PMID:In vivo disturbance of the oxidative metabolism of glucose in human cerebral gliomas. 660 89

The effect of concussion on 2-deoxy-D-glucose uptake by various regions of rat brain was investigated. The relative uptake of 2-deoxy-D-glucose was measured at 10 and 20 min post-concussion. The uptake did not change significantly from control rats at 20 min post-concussion. This may be reflective of transient nature of concussion. The uptake was higher in cortex and lower in subcortical structures at 10 min post-concussion. These changes are similar to those reported in spreading cortical depression. Spreading cortical depression may thus be a component of concussion mechanism.
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PMID:The effect of concussion on cerebral uptake of 2-deoxy-D-glucose in rat. 664 1

This study was designed to more selectively investigate the dopaminergic regulation of 18-hydroxycorticosterone (18-OHB) and aldosterone production by the adrenal zona glomerulosa. Mature rhesus monkeys received either an infusion of dopamine (2 micrograms/kg/min) or 5% dextrose (0.2 ml/min) over a 60 min period (N=6). Dopamine had no effect on plasma levels of renin activity, cortisol, corticosterone, aldosterone or blood pressure. However, dopamine suppressed (p less than 0.05) plasma 18-OHB levels from a baseline of 31.6 +/- 3.5 ng/dl to 23.6 +/- 2.1 ng/dl at 60 min after onset of infusion. This observation is in agreement with some studies in humans but differs from others in which no depression in 18-OHB was observed following dopamine infusion. Dopamine infusion markedly (p less than 0.001) suppressed plasma PRL levels by 30 min after onset of infusion. Corticosteroid responses to metoclopramide (200 micrograms/kg) after dexamethasone 1 mg im every 6 h X 5 days or placebo treatment (vehicle im every 6 h X 5 days) was then evaluated. Dexamethasone significantly suppressed basal cortisol, corticosterone, 18-OHB and aldosterone. Although dexamethasone blunted the prolactin response, it did not inhibit the aldosterone response to metoclopramide. The 18-OHB response to metoclopramide was increased (p less than 0.01) following dexamethasone treatment. Following dexamethasone suppression, 18-OHB levels were still lowered (p less than 0.05) by dopamine infusion. These results suggest that dopamine selectively inhibits zona glomerulosa production of 18-OHB and aldosterone in rhesus monkeys.
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PMID:Evidence for direct inhibitory effects of dopamine on zona glomerulosa secretion of 18-hydroxycorticosterone in rhesus monkeys. 672 68


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