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  • Ethanol  (3)
  • Lipid metabolism  (3)
  • Carbohydrate Metabolism  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 60 (1979), S. 173-176 
    ISSN: 1432-2072
    Keywords: Methamphetamine ; Swimming capaciti ; Moto behaviour ; Carbohydrate metabolism ; Lipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Swimming endurance and availability of metabolic substrates (blood glucose and nonesterified fatty acids [NEFA], liver and muscle glycogen, body fat) were studied in mice treated with 10 μg/g methamphetamine/day for 6 weeks. At the end of the 6-week treatment, motor coordination of the methamphetamine-treated animals was much better than that of controls, and swimming capacity tended to increase. While swimming, mice treated with methamphetamine mobilized more glycogen from the hepatic stores and utilized glucose more effectively. Their NEFA levels in blood were higher than those of controls. There was no difference in the muscular glycogen content.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 58 (1978), S. 161-166 
    ISSN: 1432-2072
    Keywords: Caffeine ; Swimming capacity ; Motor behaviour ; Thermoregulation ; Carbohydrate metabolism ; Lipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A comparative study of the effects of a single dose of caffeine (50 μg/g s.c.) and of 6-weeks treatment with 150 μg/g p.o. caffeine/day on swimming capacity and resistance to cold exposure was performed in mice. In contrast to acute treatment, chronic treatment with caffeine greatly reduced the swimming capacity and diminished the ability of the aminals to withstand cold stress. It could be shown by indirect means that the detrimental effect of the prolonged treatment with caffeine was not due to an accumulation of toxic levels of caffeine. Motor coordination was unaffected. There was no deficiency of metabolic substrates, since glycogen, and fat stores, and blood glucose, and fatty acid levels were not lower than in control animals. It is proposed that caffeine may interfere with the animals' ability to mobilize and spend metabolic substrates for energy requirements of skeletal muscle.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 63 (1979), S. 281-284 
    ISSN: 1432-2072
    Keywords: Fencamfamine ; Swimming capacity ; Motor behaviour ; Carbohydrate metabolism ; Lipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of long-term treatment with fencamfamine on swimming endurance and availability of metabolic substrates was investigated in mice. Fencamfamine (14 μg/g per day orally for 6 weeks) reduced maximum swimming capacity by more than 40%. This effect could not be attributed to motor incoordination or a diminution of pre-swimming levels of metabolic substrates such as liver and muscle glycogen or blood glucose and non-esterified fatty acids. However, during swimming the hepatic and muscular glycogen stores were depleted more rapidly in the fencamfamine-treated animals. Thus it appears that fencamfamine leads more rapidly to a shortage of combustible substrates in the swimming animals.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0738
    Keywords: Carbon Monoxide Poisoning ; Carbohydrate Metabolism ; Highenergy Phosphates ; Brain ; Blood Glucose ; Kohlenmonoxydvergiftung ; Kohlenhydratstoffwechsel ; Energiereiche Phosphate ; Gehirn ; Blutzucker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An weißen Mäusen wurde der Einfluß einer einmaligen (4 Std) und einer 7wöchigen, intermittierenden (35mal 9+1 mal 4 Std) Vergiftung mit Kohlenmonoxyd (0,1 Vol.- % in Luft) auf den Gehalt des Gehirns an Glykogen, Pyruvat, Lactat, ATP und Kreatinphosphat sowie den Blutzucker untersucht. Im akuten Versuch war bei einem CO-Hämoglobingehalt des Blutes von 35% der Pyruvatgehalt des Gehirns erhöht und der Blutzuckerspiegel erniedrigt. Nach 7 Wochen fanden sich bei gleichem CO-Hämoglobingehalt zusätzlich noch ein Anstieg des Lactat- und ein Abfall des Kreatinphosphatgehaltes. Die Veränderungen waren innerhalb von 15 Std Aufenthalt in CO-freier Atmosphäre nur z. T. reversibel.
    Notes: Abstract The influence of single (4 hours) or repeated (35 times, 9 hours plus once for 4 hours within a period of 7 weeks) exposure to 0.1% (v/v) carbon monoxide in air on the glycogen, pyruvate, lactate, ATP and phosphocreatine content of the brain and on the blood glucose level was investigated in mice. By a carbon-monoxyhemoglobin concentration of 35% after a single exposure to carbonmonoxide, the pyruvate content of the brain was found to be increased and the blood glucose level decreased. After 7 weeks of repeated exposure, additional changes found by the same CO-Hgb content included an increase in the lactate and a decrease in the phosphocreatine content of the brain. The changes produced by repeated carbon monoxide poisoning were found to be only partly reversibel after the animals were subsequently allowed to breathe normal air for 15 hours.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0738
    Keywords: Ethanol ; Cadmium ; Liver and kidney damage ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the combined hepatotoxic and nephrotoxic effects of cadmium and ethanol, rats maintained on an ethanol containing liquid diet (5% w/w) were given cadmium either acutely (3×1 mg/kg IP) or sub-acutely (about 14 mg/kg/day PO for 6 weeks). Parameters tested were cadmium, zinc and copper contents of blood and various organs, metallothionein (MT) contents, polysome profile of liver and kidneys, serum SDH and GPT levels and creatinine clearance. Ethanol reduced the hepatic MT contents without altering the polysome profile and the zinc and copper contents. Cadmium on the other hand raised the MT contents in liver and kidneys. This effect of cadmium predominated in the combined treatment. Morphological examination and functional tests (SDH, GPT, creatinine clearance) indicate that cadmium does not enhance the toxic effects of ethanol, and vice versa.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 302 (1978), S. 119-121 
    ISSN: 1432-1912
    Keywords: Ethanol ; Hypothalamus ; Histaminemetabolism ; Histamine-release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the rat hypothalamus, histamine content and histidine decarboxylase activity are enhanced significantly after acute administration (80–160 mg/100g body weight) of ethanol. The effects are less pronounced after chronic treatment (15% v/v in drinking water for 4 weeks). Histamine methyltransferase is unaffected in either case. In hypothalamic slices preloaded with3H-histamine and superfused with amine free solution the basal and K+-induced efflux of3H-histamine are inhibited by alcohol. The inhibition of histamine release along with the increased levels of histamine may play an important role in the central effects of alcohol.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 273 (1972), S. 213-218 
    ISSN: 1432-1912
    Keywords: Ethanol ; Pyrazole ; Carbohydrate Metabolism ; Liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of pretreatment with 340 μg/g pyrazole i.p., an inhibitor of alcohol dehydrogenase, on the changes in the carbohydrate metabolism of the liver, as produced by 4 mg/g ethanol i.v., was investigated in mice. Pyrazole completely prevented the ethanol-induced rise of the glycerol-1-phosphate content and of the glycerol-1-phosphate/dihydroxyacetone phosphate and lactate/pyruvate ratios and diminished the decrease of the hepatic pyruvate and lactate contents. This suggests, that these changes are mediated by shifts in the hepatic NADH/NAD ratio occurring during alcohol oxidation. The glycogen depleting effect of ethanol was not abolished by pyrazole showing that this effect is brought about—at least in part—by ethanol itself.
    Type of Medium: Electronic Resource
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