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)

On demand intravenous naloxone reverses respiratory depression following epidural morphine but does not have any effect on analgesia. This study aimed to assess the action of a preventive naloxone infusion on the side-effects and analgesia induced by epidural fentanyl. Sixteen patients were studied. Three had isolated uncomplicated flail chest. The thirteen others had undergone thoracotomy, and were included in the protocol at least 6 h after extubation. All patients had two epidural injections, they received an intravenous infusion of either 10 micrograms.kg-1.h-1 naloxone after a 400 micrograms bolus (group F + N) or 5% dextrose (group F), which was randomly allocated. In group F, but not in group F + N PaCO2 increased from the 15th min to the 4th, and sedation occurred from the 15th min to the 6th h. A significant and similar pain relief was noted in both groups. Duration of analgesia was not statistically different in the two groups. This preventive action of intravenous naloxone on the supraspinal adverse effects of epidural fentanyl was not accompanied by a reduction in analgesia. This could lead to widespread use of this analgesic technique.
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PMID:[Effects of intravenous naloxone on the secondary effects and analgesia after epidural injection of fentanyl]. 312 76

Three chick growth assays were conducted to investigate the effects of monensin on lysine and arginine utilization in crossbred chicks (New Hampshire X Columbian). Chicks were fed either a low lysine corn-sesame meal diet containing graded increments of crystalline lysine.HCl (Assay 1) or an arginine-deficient casein-dextrose diet (Assay 2) supplemented with graded levels of L-arginine.HCl in the presence or absence of supplemental monensin (121 mg/kg). Based upon analysis by slope-ratio methodology (i.e., gain regressed on supplemental amino acid intake), the efficiency of L-lysine or L-arginine utilization was found to be the same in both monensin-fed and control chicks. In Assay 3, effects of monensin on the lysine-arginine antagonism were studied. Chicks were fed an arginine-deficient casein-dextrose diet supplemented with 1 or 2% L-lysine.acetate in the presence or absence of supplemental monensin. Growth performance was depressed by feeding both levels of supplemental L-lysine.acetate. Monensin had no effect on the magnitude of the growth depression caused by supplemental lysine. These results support the view that neither lysine nor arginine utilization is impaired by feeding monensin.
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PMID:In vivo utilization of lysine and arginine in young chicks fed monensin. 313 6

The effect of piracetam (a putative enhancer of cerebral metabolism) on regional CMRGlu was studied by positron emission tomography of 2[18F]-fluoro-2-deoxy-D-glucose in nine patients with Alzheimer's disease, and in seven cases with multiinfarct dementia or unclassified dementia. In Alzheimer's disease, i.v. administration of piracetam, 6 g b.i.d. for 2 weeks, significantly improved rCMRGlu in most cortical areas, whereas no effect on CMRGlu of the drug was observed in the multiinfarct dementia/unclassified dementia groups. These results lend further support to the notion that adjuvant piracetam treatment is of benefit in Alzheimer's disease. They may also indicate that the typical metabolic depression in Alzheimer's disease is caused by complex interaction of disturbed transmitter and cellular function rather than by a specific deficit in the cholinergic system alone.
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PMID:Effect of piracetam on cerebral glucose metabolism in Alzheimer's disease as measured by positron emission tomography. 326 May 97

To determine the safety, efficacy, and the ventilatory responses to carbon dioxide (CO2) of mini-dose intrathecal morphine, 33 healthy women who underwent cesarean section with spinal anesthesia using 0.75% bupivacaine in 8.25% dextrose were studied. Patients were randomly assigned to receive, in a double-blind fashion, either morphine 0.25 mg (group I, n = 11), morphine 0.1 mg (group II, n = 10), or saline (group III, placebo group, n = 12) in 0.5 ml volume mixed with the bupivacaine. In both groups I and II excellent postoperative analgesia with long duration was obtained (27.7 +/- 4.0 and 18.6 +/- 0.9 hours, respectively, X +/- SEM). All patients in group III required an analgesic (8 mg subcutaneous morphine) within 3 hours of spinal anesthesia. Seven patients in group I and four patients in group II developed mild pruritus that did not require treatment. Ventilatory responses to CO2 showed no evidence of depression attributable to either the 0.25 or 0.1 mg of morphine, but significant depression of the CO2 responses was observed in group III patients after administration of subcutaneous morphine. It is concluded that a dose as low as 0.1 mg of intrathecal morphine gives excellent analgesia with minimal to no side effects and that subcutaneous morphine is associated with marked depression of the ventilatory variables.
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PMID:Mini-dose intrathecal morphine for the relief of post-cesarean section pain: safety, efficacy, and ventilatory responses to carbon dioxide. 327 78

Three experiments were conducted to evaluate the influence of dietary protein source on the monensin response in healthy chicks fed diets varying in CP. The interrelationship between dietary CP level and four different anticoccidial drugs was evaluated in a fourth experiment. The experiments were conducted from 8 to 21 or 22 days posthatching. In Experiment 1, crossbred chicks were fed corn-soybean meal (SBM) diets containing either 24 or 16% CP or casein-dextrose diets containing 20, 15, or 10% CP in the presence or absence of 160 mg/kg monensin. When CP level was decreased in the corn-SBM treatments, the resulting monensin-induced growth depression was greater. However, this interaction was not observed in chicks fed casein-dextrose diets. Experiments 2 and 3 were conducted to determine if the monensin-protein level interrelationship is influenced by the source of dietary soybean protein or by high levels of animal protein (AP). Monensin at 140 mg/kg produced a much greater growth depression at 16 than at 24% CP in chicks fed a corn-SBM diet, whereas amounts of monensin depression in chicks fed a corn-isolated soy protein diet were similar for both CP levels. As dietary protein was reduced from 24 to 16% in Experiment 3, 140 mg/kg monensin caused growth depressions of 10 and 40%, and 14 and 28%, respectively, in broiler chicks fed corn-SBM and corn-AP diets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Further investigation of the dietary protein level-monensin interrelationship in broiler chicks: influence of dietary protein source and type of anticoccidial drug. 340 44

A guideline for the preparation of peripherally administered antibiotics in fluid-restricted patients was developed. A maximum osmolality of 560 mOsmol/kg was selected since this corresponds to the theoretical osmolality of dextrose 5% in NaCl 0.9%, a solution commonly administered peripherally without significant incidence of phlebitis. Percentage concentrations corresponding to 560 mOsmol/kg of 26 intravenous antibiotics were calculated using sodium chloride equivalents. The antibiotics were reconstituted using sterile water, dextrose 5%, and NaCl 0.9% to provide an osmolality of 560 mOsmol/kg. The resulting solutions were measured for osmolality using a freezing-point depression osmometer. A total of 78 solutions were prepared and measured in triplicate. Of the 78 measured osmolalities, 67 (86 percent) were within 20 percent of the desired 560 mOsmol/kg. Only two osmolalities were more than 10 percent above the projected value. The percentage concentrations of 26 antibiotics in three solutions corresponding to 560 mOsmol/kg are presented. A method is also provided for tailoring concentrations to achieve desired osmolalities other than 560 mOsmol/kg.
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PMID:Concentration guidelines for parenteral antibiotics in fluid-restricted patients. 342 65

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-narcotic analgesics. Problems of overdosage. 355 83

6-Methylmercaptopurine ribonucleoside (6-MMPR), an inhibitor of purine nucleotide biosynthesis de novo, was used as a model compound to evaluate the relationship between the levels of intracellular guanosine triphosphate (GTP) and the formation of cellular glycoproteins and their dolichol-oligosaccharide precursors in Sarcoma 180 cells. Previous studies using the purine antimetabolite, 6-thioguanine (6-TG), demonstrated a relationship between the drug-induced decrease in GTP levels and the incorporation of radiolabelled mannose and fucose into cellular glycoproteins; estimation of the importance of these cell-surface alterations to the cytotoxicity produced by this agent was complicated by the incorporation of 6-TG nucleotides into cellular DNA and RNA. In this report, evidence is presented to show that the toxicity of 6-MMPR to Sarcoma 180 cells is associated with the effects of this agent on the intracellular pools of purine nucleotides. GTP functions in part in the activation of the sugar mannose, a step necessary for the biosynthesis of glycoproteins from nucleotide sugar precursors. Thus, 6-MMPR, which blocks the de novo pathway of purine nucleotide biosynthesis, caused a pronounced decrease in the intracellular pools of GTP in Sarcoma 180 cells; this phenomenon was accompanied by a marked reduction in the incorporation of radiolabelled mannose into cellular glycoproteins and their dolichol-linked oligosaccharide precursors. In contrast, the incorporation of glucosamine, a sugar not metabolically activated by GTP, into glycoproteins, and of leucine into protein, were depressed only after prolonged incubation with either 6-MMPR or 6-TG. Adenine restored purine nucleotide pools depleted by 6-MMPR and partially prevented both the reduction in mannose incorporation into glycoprotein and the cytotoxic effects of this antimetabolite. Guanosine partially reversed the effects of 6-MMPR on intracellular GTP pools and mannose incorporation but not the depression of ATP pools produced by this anti-metabolite. However, guanosine did not reverse the cytotoxicity of 6-MMPR but instead enhanced its toxicity. The findings are consistent with the possibility of membrane changes being involved in the cytotoxicity of 6-MMPR, but clearly other factors are involved as well.
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PMID:Inhibition of mannose incorporation into glycoproteins and dolichol-linked intermediates of Sarcoma 180 cells by 6-methylmercaptopurine ribonucleoside. 358 54

Focal cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. By a triple-tracer technique, cerebral glucose utilization, glucose content, and blood flow were simultaneously determined. Computer-assisted autoradiography revealed a core of dense ischemia in the lateral two-thirds of the striatum. A border zone of increased 2-deoxy-D-glucose (DG) uptake surrounded the ischemic insult in the acute stage. The lumped constant was increased only moderately in the border zone. Therefore, the enhanced DG uptake reflected increased glucose consumption. CBF was reduced to 20-30% in the cortical border, while minor depression and in some animals hyperemia were evident in the striate border. Six hours after the insult, the border zones of increased glucose consumption had disappeared in half the animals. In no animals examined after 20 h was glucose consumption enhanced. The study indicated a stable metabolic response to a reproducible focal insult. We conclude that continued enhancement of glucose consumption in marginally perfused areas indicates neuronal damage.
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PMID:Focal ischemia of the rat brain: autoradiographic determination of cerebral glucose utilization, glucose content, and blood flow. 373 1

The safe clinical use and physical stability of a total nutrient admixture (TNA) system containing a soybean oil emulsion (Intralipid) has been reported. A study was conducted to compare the physical stability of four admixtures which were divided into two groups based upon the ratios (1:1:1 and 2:1:1) of amino acids (8.5%), dextrose (70%), and fat emulsion (20%). The fat component in each group contained either a new soy bean fat emulsion, Soyacal, or Intralipid. The quantities of all electrolytes, trace elements and vitamin additives were the same. All solutions were stored at 4 degrees C for 28 days and then held at ambient temperature for 5 days for a total 33-day study period. Each admixture was serially analyzed on days 0, 1, 2, 3, 5, 7, 14, 21, 28, 29, 30, 31, 32, and 33. Examination of gross visual appearance and determinations of pH were performed. Osmolality was measured by means of freezing point depression (Advanced Digimatic Osmometer, Advanced Instruments, Inc., Needham Heights, MA). A Brookhaven particle analyzer was used to measure lipid particle size and particle size distribution. Electron and light microscopy were used to verify maximum particle size and distribution on days 0, 7, 14, 21, 28, and 29. The type of lipid emulsion used did not affect the pH or osmolality of the admixtures. Admixtures prepared with the 2:1:1 ratio had slightly higher pH (0.07) and lower osmolality (350 mOsm/kg). The range of mean diameters for the admixtures prepared with Soyacal and Intralipid were 0.283 to 0.310 micron and 0.314 to 0.351 micron, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of total nutrient admixture stability using two intravenous fat emulsions, Soyacal and Intralipid 20%. 374 94


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