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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 186 (1986), S. 353-363 
    ISSN: 1433-8580
    Keywords: Ammonia metabolism ; Glutamine metabolism ; Kidney ; Muscle ; Gut
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to investigate the influence of acid and alkali food supplementation on systemic ammonemia to explain the hyper-ammonemia previously observed in rats fed a high protein diet. In normal rats, arterial ammonia concentration significantly increases after 4 days of HCl-supplemented diet. Following a NaHCO3-enriched food, there is only a slight but not significant decrease in arterial ammonia level. These changes occur before any variation in arterial acid-base status and are of renal origin. Indeed, there is a positive linear correlation (r = 0.946;P 〈 0.001) between arterial ammonia level and the ammonia concentration difference between the renal vein and artery (which varies proportionally to the urinary ammonium excretion). Hindquarter uptake and intestinal release of ammonia do not significantly participate in the arterial ammonia changes observed. Following HCl-enriched diets, increased renal glutamine uptake, enhanced hindquarter glutamine release, and perhaps decreased intestinal glutamine uptake occur simultaneously. In conclusion, acid and alkali food supplementation intervenes on the renal ammonia release into the circulation with concomitant arterial ammonemia changes.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Rat ; ammonium infusion ; blood ammonia ; glucose metabolism ; plasma immunoreactive insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to explain the abnormalities of glucose metabolism previously observed in patients with blood ammonia elevation, the effect of a transitory hyperammonemia on I. V. glucose tolerance was investigated in rats. An I. V. glucose tolerance test was performed in 3 groups of 15 rats 60 min after the beginning of a 95 min infusion of either a 2 ml isotonic NaCl solution (control group) or ammonium acetate solutions at low (0.50 μmol/kg/min. NH4+) or high doses (1.70 μmol/kg/min NH4+). The “high” NH4+infusion produced an increase of blood ammonia to levels near 1000 μg/100 ml, a significant decrease in the K coefficient for glucose disappearance (2.53 × 10−2±0.20 compared to 4.92 × 10−2±0.13 in control group) and a suppression of the radioimmunological plasma insulin (I.R.I.) response to glucose. With the “low” NH4 + infusion the hyperammonemia was less pronounced (200–300 μg/100 ml), but the decrease in K(3.02 × 10−2±0.15) and in the first phase of I.R.I, release remained significant. The decrease in glucose disappearance rate could be accounted for by the proportional decrease in insulin secretion. Thus glucose intolerance induced by ammonium acetate infusions may be due to a direct effect of NH4 + on the pancreas. These abnormalities in glucose metabolism depend on the quantity of infused ammonium.
    Type of Medium: Electronic Resource
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