Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Intravenous infusion of the individual components of the renin-angiotensin system caused drinking in dogs in water balance. 2. Angiotensin II was the most potent and rapidly acting peptide inducing drinking. The minimum effective rate of infusion was between 8.3 and 16.6 X 10(-12) mole kg-1 min-1 which yield blood levels of angiotensin II that fell well within physiological limits for the dog and were mildly pressor. Angiotensin I and synthetic renin substrate caused less drinking than angiotensin II, and angiotensin III was the least effective dipsogen. 3. Renin caused significant drinking when infused I.V. at a rate of 0.5 u. min-1 for 15 min. Drinking was slower in onset and continued for longer than after other components of the renin-angiotensin system. 4. Within the dose range 1875-15,000 X 10(-12) mole of angiotensin II the amount of water drunk depended more on the rate of infusion than on the duration of the infusion. 5. During an I.V. infusion of angiotensin II lasting 2 hr, the rate of drinking was greatest during the first 15 min. After this declined progressively. 6. A delay of 1 hr after the start of an intravenous infusion of angiotensin II before access to water was allowed, did not significantly reduce the amount of water drunk. Nor did infusion of isotonic saline for 105 min reduce drinking in response to a subsequent infusion of angiotensin II. However, a preload of dilute milk approximately equal in volume to the amount of water normally drunk in response to I.V. angiotensin II significantly reduced drinking. Therefore the dog stopped drinking during long-term infusions of angiotensin II owing to the action of satiety mechanisms and not to tachyphylaxis or fatigue. 7. Intracarotid infusion of angiotensin II, angiotensin I, synthetic renin substrate and angiotensin III, at 40 X 10(-12) mole min-1 also caused drinking. Intakes of water were similar to the intakes after I.V. infusion at six times the arterial rate, except that angiotensin I was relatively less effective by intracarotid infusion than by I.V. infusion. 8. Renin, infused at 0.5 u. min-1 for 15 min, was much less effective by intracarotid infusion than by intravenous. 9. These results are compatible with a role for circulating angiotensin II in the thirst of hypovolaemia or moderate extracellular dehydration.
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PMID:Systemic angiotensin-induced drinking in the dog: a physiological phenomenon. 65 Apr 70

The Isoparaffins covered in this manuscript are branched aliphatic hydrocarbons with a carbon skeleton length ranging from approximately C10 to C15. They are used in the manufacture of liquid imaging toners, paint formulations, charcoal lighter fluid, furniture polishes and floor clearners. Potential exposure exists in the petroleum, printing and paint industries. Isoparaffins have a very low order of acute toxicity, being practically non-toxic by oral, dermal and inhalation routes. However, aspiration of liquid isoparaffins into the lungs during oral ingestion could result in severe pulmonary injury. Dermally, isoparaffins have produced slight to moderate irritation in animals and humans under occluded patch conditions where evaporation cannot freely occur. However, they are not irritating in non-occluded tests, which are a more realistic simulation of human exposure. They have not been found to be sensitizers in guinea pig or human patch testing. However, occasional rare idiosyncratic sensitization reactions in humans have been reported. Instillation of isoparaffins into rabbit eyes produces only slight irritation. Several studies have evaluated sensory irritation in laboratory animals or odor or sensory response in humans. When evaluated by a standard procedure to assess upper airway irritation, isoparaffins did not produce sensory irritation in mice exposed to up to 400 ppm isoparaffin in air. Human volunteers were exposed for six hours to 100 ppm isoparaffin. The subjects were given a self-administered questionnaire to evaluate symptoms, which included dryness of the mucous membranes, loss of appetite, nausea, vomiting, diarrhea, fatigue, headache, dizziness, feeling of inebriation, visual disturbances, tremor, muscular weakness, impairment of coordination or paresthesia. No symptoms associated with solvent exposure were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicology update isoparaffinic hydrocarbons: a summary of physical properties, toxicity studies and human exposure data. 219 78

The aim of the present study was to investigate the metabolic base of psychoneurological symptoms, most notably tiredness and loss of concentration ability, appearing after carbohydrate-rich meals and during oral glucose tolerance tests. Such metabolic changes may be the cause of many accidents attributed to the "human factor". Oral glucose tolerance tests (OGTT) were performed in healthy volunteers, divided into symptomatic (n = 21) and symptom-free (n = 15) groups. Since the symptoms arising during OGTT simulate those in alcohol intoxication, a method for clinical examination of alcohol intoxication was used to separate symptom-free from symptomatic subjects. Comparison of blood glucose concentrations during OGTT revealed the symptomatic group to have higher concentrations in blood samples taken 15 min (p less than 0.05), 30 min (p less than 0.01), 45, 60 and 90 min (p less than 0.05) after intake of glucose than those having no symptoms. The symptoms began when the glucose concentration was at maximum, some 38 min (mean value) following the ingestion of glucose. The symptomatic subjects demonstrated a normal assimilation rate of glucose (mean 1.7 %/min) as tested with intravenous glucose tolerance tests and the differences in blood glucose concentrations between the groups is concluded to depend on the rate of absorption of glucose from the intestinal tract. The enterochromaffine cells of the intestinal tract are the site of biosynthesis, storage and release of 5-hydroxytryptamine (5-HT) (serotonin). In whole blood practically all of the 5-HT is of thrombocytic origin. Thrombocytes are thought to be peripheral models of 5-HT neurons in regard to 5-HT uptake, storage release and metabolism. Thrombocytes have a mechanism for 5-HT uptake analogous to the reuptake mechanism for 5-HT in the serotonergic nerve terminals. The whole blood 5-HT changes parallel changes in the 5-HT concentrations of the neurons. In this work 5-HT concentrations were measured during OGTT in whole blood to ascertain the possible relation between 5-HT changes and glucose absorption. For this purpose a reliable, fluorometric method for 5-HT was developed with the following improvements: In whole EDTA-blood the oxidation of 5-HT was prevented with ascorbic acid. The oxidation of hemoglobin iron to ferri-iron was prevented with carbon monoxide, because 5-HT, being a phenol, will otherwise form a complex with ferri-iron. Proteins were precipitated with perchloric acid and the supernatant neutralized before purification of 5-HT by cation exchange.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of 5-hydroxytryptamine (serotonin) in oral glucose intolerance. 658 28

Alcohol intoxication and hangover were studied in 12 healthy male subjects who participated in three 18-h experimental sessions; two sessions in which they consumed 1.43 g alcohol/kg body weight as mixed beverages together with food, and one control session when mineral water was substituted for the alcoholic beverages. In one of the alcohol sessions they received chlormethiazole, 1 g at bedtime and 0.5 g early the following morning, in the other, they were given placebo tablets. The following variables were studied: blood-alcohol concentration; blood pressure; heart rate; blood lactate; blood pyruvate; urinary catecholamines (only during hangover); psychomotor and cognitive capacities; as well as subjective reactions. During intoxication, heart rate and lactate-pyruvate ratio were significantly increased and performance efficiency was significantly deteriorated in comparison with the control condition. During hangover, heart rate, blood pressure, and lactate-pyruvate ratio were significantly elevated, and cognitive performance was still affected, in some tests to a significant degree. During this stage there was a great variation between subjects as regards subjective hangover. Chlormethiazole was found to lower blood pressure and adrenaline output and, furthermore, to relieve unpleasant physical symptoms, but did not affect fatigue and drowsiness. The cognitive test results were only slightly influenced by this agent, while psychomotor performance was significantly impaired. Subjects with severe subjective hangover seemed to benefit more from the chlormethiazole treatment than subjects with a mild hangover.
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PMID:Alcohol intoxication and hangover: modification of hangover by chlormethiazole. 677 3

Development of the fatigue state in rats, subjected to prolonged alcohol intoxication, after swimming with might led to dissimilar alterations in the system of ammonia formation and binding in brain and spinal cord as compared with control animals under the same conditions of loading. Within the first minutes of the heavy loading the faster and more distinct accumulation of ammonia was observed, then the rapid exhaustion of the reaction occurred and the ammonia production was markedly decreased in the state of fatigue. Impairments in brain protein deamidation and decrease in content of urea were found. At the same time, dynamics of gamma-aminobutyric acid, dicarboxylic amino acids and their amides was altered.
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PMID:[Brain and spinal cord nitrogen metabolism in chronic alcoholism following strenuous physical exertion]. 719 7

Acute and chronic alcohol intoxication causes a considerable deamidation of central nervous system proteins which is most pronounced in the spinal cord. There occurs rearrangement in the amide bonds lability and in the ratio of easy-hydrolyzable and strongly bound amide groups. The metabolic response to the single administration of ethanol is disturbed. Alcohol intoxication causes changes in the amount of amide groups in the central nervous system proteins under conditions of physical exercises and fatigue development.
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PMID:[Amide groups of brain and spinal proteins in acute and chronic alcohol intoxication]. 719 2

A double blind cross-over design trial was carried out to investigate the effect of simultaneous administration of alcohol (0.5 g/kg) and ritanserin (10 mg) on biological and behavioral functioning. Twenty healthy volunteers were selected to participate in the study. To assess the effect of treatments the following evaluations were performed: psychomotor tests, vital signs, intoxication, euphoria, and mood. In addition, ritanserin and alcohol plasma concentration were measured. Psychomotor performance and vital signs during the ritanserin session did not differ significantly from the placebo session. Similar results were obtained in regard to alcohol intoxication, euphoria, and mood, except for tiredness and alertness, which were significantly different compared to placebo. Differences in blood alcohol concentration between the ritanserin and the placebo sessions did not attain significance. Plasma ritanserin concentration was 143 ng/ml 1 h after alcohol administration and decayed to 53 ng/ml 6 h after alcohol consumption in the active treatment session. Our findings tend to indicate that ritanserin neither enhances the central nervous system depressant effect of alcohol nor produces a pharmacokinetic interaction during acute alcohol ingestion.
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PMID:Single-dose ritanserin and alcohol in healthy volunteers: a placebo-controlled trial. 859 Jun 16

The opiate antagonist naltrexone (NTX) blocks relapse drinking in alcoholics and modifies some of the subjective effects of alcohol intoxication. Benzodiazepines have demonstrated cross-dependence and cross-tolerance to alcohol. Furthermore, benzodiazepine intoxication has effects on mood and psychomotor performance that are similar to alcohol intoxication. The effects of NTX on diazepam intoxication were investigated in non-drug abusing individuals. Eighteen men and eight women were randomly assigned to receive either 50 mg NTX or placebo PO, on two different occasions in a within-subjects, crossover, double-blind protocol. Diazepam was taken by mouth, 90 min after NTX. At -90, 45, 75, 135, 210 min, subjects were tested with repeated assessments of several mood and sensation scales and a computer-generated psychomotor test battery (CTB). Blood samples were also obtained and analyzed for serum diazepam levels. Diazepam induced several sensations and mood effects similar to those induced by alcohol. Negative mood states such as sedation, fatigue, and anxiety were higher for NTX than for placebo. Positive mood states such as friendliness, vigor, liking the effects of diazepam, and feeling high from diazepam were all lower for NTX than for placebo. There were no group differences on the CTB performance. NTX delayed the time to reach peak diazepam levels, so that peak levels occurred at 75 min for placebo compared to 135 min for NTX. A sub-analysis was conducted with 14 subjects who were FHP for alcoholism, but no differences were found on these outcome measures.
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PMID:Naltrexone effects on diazepam intoxication and pharmacokinetics in humans. 949 28

In 1992, an outbreak of chronic diarrhea occurred among passengers on a cruise ship visiting the Galapagos Islands, Ecuador. Passengers (548) were surveyed, and stool and biopsy specimens from a sample who reported chronic diarrhea were examined. On completed questionnaires, returned by 394 passengers (72%), 58 (15%) reported having chronic diarrhea associated with urgency (84%), weight loss (77%), fatigue (71%), and fecal incontinence (62%). Illness began 11 days (median) after boarding the ship and lasted 7 to >42 months. Macroscopic and histologic abnormalities of the colon were common, but extensive laboratory examination revealed no etiologic agent. No one responded to antimicrobial therapy. Patients were more likely than well passengers to have drunk the ship's unbottled water or ice before onset of illness and to have eaten raw sliced fruits and vegetables washed in unbottled water. Water handling and chlorination on the ship were deficient. Outbreaks of a similar illness, Brainerd diarrhea, have been reported in the United States. Although its etiology remains unknown, Brainerd diarrhea may also occur among travelers.
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PMID:An outbreak of Brainerd diarrhea among travelers to the Galapagos Islands. 953 80

The present study systematically compared the effects of fatigue and alcohol intoxication on a range of neurobehavioural tasks. By doing so, it was possible to quantify the performance impairment associated with fatigue and express it as a blood alcohol impairment equivalent. Twenty-two healthy subjects aged 19-26 years participated in three counterbalanced conditions. In the sustained wakefulness condition, subjects were kept awake for 28 h. In the alcohol and placebo conditions, subjects consumed either an alcoholic or non-alcoholic beverage at 30 min intervals, until their blood alcohol concentration reached 0.10%. In each session, performance was measured at hourly intervals using four tasks from a standardised computer-based test battery. Analysis indicated that the placebo beverage did not significantly effect mean relative performance. In contrast, as blood alcohol concentration increased performance on all the tasks, except for one, significantly decreased. Similarly, as hours of wakefulness increased performance levels for four of the six parameters significantly decreased. More importantly, equating the performance impairment in the two conditions indicated that, depending on the task measured, approximately 20-25 h of wakefulness produced performance decrements equivalent to those observed at a blood alcohol concentration (BAC) of 0.10%. Overall, these results suggest that moderate levels of fatigue produce performance equivalent to or greater than those observed at levels of alcohol intoxication deemed unacceptable when driving, working and/or operating dangerous equipment.
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PMID:Quantifying the performance impairment associated with fatigue. 1064 65


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