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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 36 (1993), S. 813-816 
    ISSN: 1432-0428
    Keywords: Endogenous acid production ; intracellular pH ; insulin ; metabolic acidosis ; Na+/H+ antiporter ; PCO2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin is the cornerstone of therapy for diabetic ketoacidosis because it causes the rate of ketoacid production to fall; this action takes several hours to occur. Insulin also causes H+ to be transported from the intracellular fluid to the extracellular fluid in vitro. The purpose of this study was to determine if insulin led to the acute export of H+ from the intracellular fluid in vivo. If so, we wished to determine if this also occurred during chronic metabolic acidosis, to quantitate the magnitude of the H+ shift, and to evaluate the mechanisms involved. The administration of low- or high-dose insulin to normal dogs and high-dose insulin to dogs with chronic metabolic acidosis caused the concentration of bicarbonate in plasma to decline by close to 3 mmol/l. The PCO2 fell by close to 15 % in all three groups of dogs, so one component of the fall was due to hyperventilation. As the pH of blood did not change, a primary metabolic acidosis also occurred. The fall in bicarbonataemia was not due to net accumulation of organic acids or to a loss of bicarbonate or organic anions in the urine. Taken together, insulin, when given at doses used to treat diabetic ketoacidosis, might induce a significantly greater degree of acidaemia in the extracellular fluid acutely after it is given.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary A large number of compounds were tested for their effectiveness as inhibitors of the tricarboxylate and dicarboxylate transporting systems of rat liver mitochondria as monitored by citrate/[14C] citrate exchange and phosphate/[14C]l-malate exchange, respectively. The influence of inhibitor structure on inhibitory potency is discussed for each transporting system and deductions made concerning the nature of the binding sites of these carrier systems.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 223 (1969), S. 1369-1371 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Fig. 1. Polarographic measurements of oxygen consumption of white adipose tissue mitochondria with citrate, isocitrate and 2-oxoglutarate as substrates. Adipose tissue mitochondria (1 mg protein) were suspended in 3 ml. of a medium containing 125 mM KC1, 20 mMZm chloride, #H 7-4, 1-6 mM inorganic ...
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-198X
    Keywords: Key words: Renal tubular acidosis ; Osteopetrosis ; Carbonic anhydrase II deficiency ; Bicarbonate reabsorption ; Ammonium excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Renal tubular acidosis with osteopetrosis is an autosomal recessive disorder due to deficiency of carbonic anhydrase II (CAII). A 3.5-year-old Egyptian boy with osteopetrosis and cerebral calcification had a persistent normal anion gap type of metabolic acidosis (plasma pH 7.26) and a mild degree of hypokalemia. A baseline urine pH was 7.0; ammonium (NH4 +) excretion was low at 11 μmol/min per 1.73 m2; fractional excretion of bicarbonate HCO3 (FEHCO3) was high at 9%, when plasma HCO3 was 20 mmol/l; citrate excretion rate was high for the degree of acidosis at 0.35 mmol/mmol creatinine. Intravenous administration of sodium bicarbonate led to a urine pH of 7.6, a FEHCO3 of 14%, a urine-blood PCO2 difference of 7 mmHg, NH4 + excretion fell to close to nil, and citrate excretion remained at 0.38 mmol/mmol creatinine. Intravenous administration of arginine hydrochloride caused the urine pH to fall to 5.8, the FEHCO3 to fall to 0, the NH4 + excretion rate to rise to 43 μmol/min per 1.73 m2, and citrate excretion to fall to 〈0.01 mmol/mmol creatinine. These results show that our patient had a low rate of NH4 + excretion, a low urine minus blood PCO2 difference in alkaline urine, and a low urinary citrate excretion, but only when he was severely acidotic. He failed to achieve a maximally low urine pH. These findings indicate that his renal acidification mechanisms were impaired in both the proximal and distal tubule, the result of his CAII deficiency.
    Type of Medium: Electronic Resource
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