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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Driving a car is a complex psychomotor and perceptual task which is subject to impairment by many factors. Several workers have studied the potential effects of drugs and alchol in crash production by epidemiological and laboratory studies. Both types of studies have yielded useful data but their limitations must be borne in mind when applying the results in pratice. Alcohol is obviously the most common single cause of traffic accidents. A progessively increased risk with increasing blood alcohol levels is well documented; fatigue and/or drugs increase this risk. Drugs are related much more infrequently to traffic accidents although on the basis of statistics, there is a potential risk with drug use. However, drugs alone are not as important as alcohol. The most significant drugs as regards driving risk are obviously certain antianxiety agents, hypnotics, stimulants, hallucinogens, marihuana, lithium and narcotic analgesics, as well as ganglionic blocking agents, insulin and sulphonylurea derivates. Patients should not drive after taking these drug until they are objectively fully alert and capable. Anticholinergics, antihistamines, antidepressants, antipsychotics, phenybutazone, indomethacin, alpha-methyldopa, and beta-blockers may in some cases cause central side effects (e.g. drowsiness) strong enough to affect driving performance. After starting therapy with these drugs, or after a significant change in dose, driving should be avoided until it is known that unwanted effects do not occur. Psychotropic drugs may enhance the deleterious effect of alcohol, and with most hypnotics there is still an effect the next morning. Some drugs (e.g. anticonvulsants or antiparkinsonian drugs) may make driving safer, but the disease (epilepsy, Parkinsonism, cardiovascular diseases, psychic disorders, etc.) ofter precludes driving. Clinicians should warn their patients about an impairment of driving skills if this is likely to occur due to the drug or the illness concerned.
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PMID:Drugs, alcohol and driving. 3 67

The EEG was recorded in 27 subjects during hangover. Male healthy volunteers drank 1.75 g/kg body weight of ethanol in 3 h and the EEG was recorded 14-16 h later when the degree of hangover was highest. For control purposes a second EEG was recorded after a similar session when subjects drank water instead of ethanol. A third record was taken in normal laboratory conditions. T5-A1 and O1-A1 derivations were subjected to computer analysis from which spectral and frequency parameters were calculated. Visual analysis of the EEG during hangover showed a decrease and slowing of alpha activity and an increase in theta activity. Spectral analysis of the EEG gave a statistically significant increase in 7-8 c/sec activity during hangover. The EEG change could not be explained in terms of blood alcohol level, hypoglycaemia or acidosis. Also fatigue could be excluded as a cause of EEG change by means of "water controls". The conclusion is that the slowing of the EEG during hangover is caused by the depressant action of ethanol, or its metabolites, on cortical function.
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PMID:Electroencephalographic changes during experimental hangover. 5 42

The interaction between effects of ethanol ingestion and those of infrasound on neuro-muscular fatigue in the animal is abolished by ascorbic acid. The relevant mechanism is in acetaldehyde detoxification.
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PMID:[Suppression by ascorbic acid of neuromuscular fatigue due to sound-alcohol synergy]. 10 54

The effects of noise, alcohol, and the combination of the two were studied on muscular fatigue in several mouse strains to investigate a possible interaction between the two stresses. Muscular fatigue was measured by latency to submersion during a forced-swimming test. Animals were exposed to acoustic stimuli of fixed frequency and intensity for 2h preceding the test. Ethanol was administered orally from 30 min to 3h 30 min prior to testing. Alcohol doses and sound intensities were subliminal when administered separately. While no significant interaction occurred between alcohol and audible sound, the interaction between alcohol and infrasound was highly significant indicating that their joint effects are more than merely additive. Blood alcohol measurements indicate that these interactive effects are prolonged for more than 2h after elimination of alcohol from the blood. Effects are similar in genetically deaf and hearing mice, implicating involvement of nonauditory pathways.
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PMID:Reduction of swimming time in mice through interaction of infrasound and alcohol. 11 95

The effect of carbohydrates, aromatic alcohols, choline and acetylcholine on the biomass production and biosynthesis of choline esterase was studied with Arthrobacter simplex var. cholinesterasus. Fructose was found to be the best carbon source for the biomass accumulation and synthesis of choline esterase. Almost the same amount of the enzyme was produced on media with glucose and maltose as on the medium with fructose though the biomass yield was much lower. On the contrary, the biomass production was higher on media with acetylcholine and ethanol, but synthesis of the enzyme was inhibited. Choline was not assimilated by the culture. Differences in assimilation of glucose and fructose by the culture were found to depend on their concentration and the presence, or absence, of the inductor (acetylcholine) in the medium. Fructose was assimilated by the culture almost completely irrespective of its concentration and the presence of the inductor in the medium. Glucose was assimilated partly, best of all at a concentration of 0.5%. An increase of the concentration to 1% inhibited assimilation of glucose by the organism though had no effect on the biomass production and synthesis of the enzyme. The inductor stimulated assimilation of glucose by a factor of 1.5. Synthesis of choline esterase on the medium with acetylcholine at a concentration of 1% was increased more than twofold upon addition of glucose at a concentration of 0.1%. Biosynthesis of the enzyme rised with glucose concentration though accumulation of the biomass was inhibited. Inhibition of choline esterase synthesis on the medium with acetylcholine as a sole carbon source is due to a lack of energy and the absence of synthesis of carbon compounds which are acceptors of acetyl and methyl groups.
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PMID:[Effect of various carbon sources on cholinesterase formation by Arthrobacter simplex var. cholinesterasus]. 100 62

In order to estimate the combined effect of ethanol and fatigue on the activity of tendon reflexes, the mechanical threshhold and the latency of the patellar tendon, the radial and the biceps reflexes as well as the time of contraction of the musculus quadriceps femoris was investigated in men, with an ethanol level in blood at 80 mg % during elimination-period, and with tired subjects meaning that they hade done their usual daywork and had been awake for about 20 to 22 hours. The group, consisting of 21 male students, was then investigated under both these conditions. The patellar reflex was elicited by a specially constructed reflexhammer, by which the mechanical power could by measured exactly, from the angle of the position the hammer was released from and its known weight. The latency and the muscular contraction time were registered with electrodes on the skin by an oscillograph. The mechanical threshhold of the patellar, biceps and radial reflexes and the latency of there reflexes were significantly and equally impaired by ethanol as well as by fatigue. The combination of both these factors resulted in an almost exactly additional effect. The contractiontime of the m. quadriceps was prolonged more by fatigue than by ethanol. Comparing these results with fromer findings, a depressing effect of the formatio reticularis of the brainstem on the activity of the spinal motorcells is to be discussed. This impairment of neuro-muscular coordination and activity obviously is dangerous for drivers. It should especially be noted, that the effect of a wake period of 20 to 22 hours can be compared with that of a bloodlevel of 80 mg % ethanol as to the impairment of the tendon reflexes.
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PMID:[About the effect of alcohol and tiredness on the activity of tendon reflexes (author's transl)]. 121 9

Rats were acutely administered ethanol as a primed constant infusion in order to produce sustained blood ethanol levels of 8-12 or 55-65 mM. At the end of ethanol infusion the livers were either freeze-clamped in vivo or isolated and perfused for metabolic studies. The rate of gluconeogenesis and its responsiveness to phenylephrine (10 microM), prostaglandin F2 alpha (5 microM) and glucagon (10 nM), as well as the redox state of the cytosolic NAD(+)-NADH system were assessed in livers isolated from acutely ethanol-treated rats, and subsequently perfused without ethanol. For liver clamped in vivo, high- but not low-ethanol treatment decreased the ATP content by 31% and slightly increased ADP and AMP content, resulting in a decreased energy charge (11%). Glutamate and aspartate content was also increased in high-dose ethanol-infused rats with no changes in malate and 2-oxoglutarate content. Gluconeogenesis with saturating concentrations of lactate (4 mM)+pyruvate (0.4 mM) was delayed in reaching a plateau in the livers of high-dose ethanol-treated rats and its response to all three stimulators was impaired. Low-dose ethanol treatment only decreased the liver response to phenylephrine. While the perfused livers of low-dose ethanol-treated rats displayed no changes in adenine nucleotide content, the livers of high-dose ethanol-treated rats had a decreased ATP (35%) and an increased AMP (77%) content, paralleled by a fall in the total adenine nucleotides (14%) and energy charge (14%). No differences were observed between the saline- and ethanol-treated rats with respect to malate-aspartate shuttle intermediate concentration in perfused livers. Also, the livers of high-, but not low-dose ethanol-treated rats had a more negative value of NAD(+)-NADH redox state as compared to the livers of control rats. The data suggest that acute ethanol intoxication produces changes in liver metabolism and its responsiveness to hormones/agonists that are demonstrable for at least 2 hr after isolation and perfusion of the liver.
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PMID:Effects of acute alcohol intoxication on gluconeogenesis and its hormonal responsiveness in isolated, perfused rat liver. 135 76

Inhibition of endogenous long chain fatty acids oxidation by tetradecylglycidate (TDGA) impeded gluconeogenesis from lactate or from low concentrations of pyruvate (less than 0.5 mM). The inhibitory effect of TDGA was overcome by medium and short chain fatty acid or by concentrations of pyruvate about 0.5 mM, but not by 10-fold higher concentrations of lactate. Despite decreased energy demand when gluconeogenesis was inhibited by TDGA, the pyruvate-induced increase in hepatic oxygen consumption was similar to the control, indicating that pyruvate transport across the mitochondrial membrane and/or its decarboxylation was not altered, and therefore can not be responsible for the inhibition of gluconeogenesis. Neither does a deficiency of acetyl-CoA explain the decrease in the gluconeogenic flux since high pyruvate loads (greater than 0.5 mM), beta-hydroxybutyrate or even ethanol was capable of overcoming the inhibitory effect of TDGA in the absence of significant changes in the hepatic content of acetyl-CoA. At low (less than 0.3 mM), presumably physiological, pyruvate concentrations, its rate of mitochondrial utilization is limited by the activity of the monocarboxylate transporter. Agents that reduced the mitochondrial NAD system, and therefore reduced flux through pyruvate dehydrogenase, like beta-hydroxybutyrate or ethanol, stimulated gluconeogenesis when fatty acid oxidation was inhibited. The latter observations indicate that the primary role of endogenous fatty acid, when substrate availability is limiting, is to spare mitochondrial pyruvate by decreasing its oxidation, and therefore shifting the partitioning between the carboxylation and decarboxylation reactions toward the former.
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PMID:Role of endogenous fatty acids in the control of hepatic gluconeogenesis. 172 53

Blood adenine nucleotides were determined in patients with alcoholic and non-alcoholic liver diseases. They included patients with alcoholic hepatitis (AH), alcoholic liver cirrhosis (ALC), non-alcoholic liver cirrhosis (NALC), and amoebic liver abscess (ALA) (28 patients). A decrease of 28% to 39% in blood ATP levels was observed among the patients with AH and the cirrhotic groups, respectively (p less than 0.05), whereas no significant changes in blood ATP levels were detected in the ALA group. Although total blood adenine nucleotides were significantly diminished in AH, ALC, and NALC groups, the AH patients retained their energy relationships within normal range. On the other hand, the cirrhotic groups, independently of their etiology, failed to maintain an adequate ATP/ADP ratio, energy charge, and phosphorylation potential in the blood, suggesting a decreased energy availability in their blood cells. Nevertheless, the mechanism involved in these effects remains to be elucidated, a failure of the damaged liver to supply purines to extra-hepatic tissues might be a major event altering the blood energy parameters.
Alcohol Clin Exp Res 1991 Jun
PMID:Alterations of ATP levels and of energy parameters in the blood of alcoholic and nonalcoholic patients with liver damage. 187 35

Ethanol sensitivity is a syndrome of flushing, tachycardia, weakness, fatigue, and other dysphoric symptoms in response to relatively small doses of ethanol. We describe a case of extreme ethanol sensitivity presenting with coma and review the pathophysiology of the syndrome.
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PMID:Ethanol sensitivity. 192 88


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