Observations on the Rôle of Tissues in Maintaining the Acid-Base Equilibrium of the Blood

Banus, M. Garcia; Katz, Louis N.

doi:10.1152/ajplegacy.1927.81.3.644

Cited by 6 publications

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“…Levitt et al (1956) found an increase in bone Cl − when HCl or NH 4 Cl solutions were infused into rats. However, in other experiments, no changes were detected in bone Cl − (Bergstrom and Wallace, 1954) or the additional Cl − could be accounted for by changes in ECF Cl − and changes in red blood cell intracellular Cl − (Banus andKatz, 1927, Swan et al, 1955;Tobin, 1956). Despite evidence for excess Cl − in the bone hydration shell, it is uncertain if the concentration would increase with increased retention of Cl − or metabolic acidosis in the pig.…”

Section: Discussionmentioning

confidence: 95%

Chronic metabolic acid load induced by changes in dietary electrolyte balance increased chloride retention but did not compromise bone in growing swine

Budde

Crenshaw

2003

Journal of Animal Science

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The effects of chronic dietary acid loads on shifts in bone mineral reserves and physiological concentrations of cations and anions in extracellular fluids were assessed in growing swine. Four trials were conducted with a total of 38 (8.16 +/- 0.30 kg, mean +/- SEM) Large White x Landrace x Duroc pigs randomly assigned to one of three dietary treatments. Semipurified diets, fed for 13 to 17 d, provided an analyzed dietary electrolyte balance (dEB, meq/kg diet = Na+ + K+ - Cl-) of -35, 112, and 212 for the acidogenic, control, and alkalinogenic diets, respectively. Growth performance, arterial blood gas, serum chemistry, urine pH, mineral balance, bone mineral content gain, bone-breaking strength, bone ash, and percentage of bone ash were determined. Dietary treatments created a range of metabolic acid loads without affecting (P > 0.10) growth or feed intake. Urine pH was 5.71, 6.02, and 7.65 +/- 0.48 (mean +/- SEM) and arterial blood pH was 7.478, 7.485, and 7.526 +/- 0.006 for pigs fed acidogenic, control, and alkalinogenic treatments, respectively. A lower dEB resulted in an increased (P < 0.001) apparent Cl- retention (106.6, 55.4, and 41.2 +/- 6.3 meq/d), of which only 1.6% was accounted for by expansion of the extracellular fluid Cl- pool as calculated from serum Cl- (105.5, 103.4, 101.6 +/- 0.94 meq/L (mean +/- SEM) for pigs fed acidogenic, control, and alkalinogenic treatments, respectively. A lower dEB did not decrease (P > 0.10) bone mineral content gain, bone-breaking strength, bone ash, percentage of bone ash, or calcium and phosphate balance. In conclusion, bone mineral (phosphate) was not depleted to buffer the dietary acid load in growing pigs over a 3-wk period.

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Section: Discussionmentioning

confidence: 95%

Chronic metabolic acid load induced by changes in dietary electrolyte balance increased chloride retention but did not compromise bone in growing swine

Budde

Crenshaw

2003

Journal of Animal Science

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“…Dottenveich (1933) showed that the calciferous glands of earthworms were capable of giving up calcium to buffer carbon dioxide accumulating in body fluids. Banus and Katz (1927) found weak buffering by hind leg muscles of a cat.…”

Section: Calcium Contentmentioning

confidence: 95%

The Role of Tissues in the Anaerobic Metabolism of the Mussel Anodonta Hallenbeckii Lea

Culbreth¹

1941

The Biological Bulletin

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The participation of the carbonates of bone in the neutralization of ingested acid

Irving

Chute

1932

J. Cell. Comp. Physiol.

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Observations on the Rôle of Tissues in Maintaining the Acid-Base Equilibrium of the Blood

Cited by 6 publications

References 0 publications

Chronic metabolic acid load induced by changes in dietary electrolyte balance increased chloride retention but did not compromise bone in growing swine

Chronic metabolic acid load induced by changes in dietary electrolyte balance increased chloride retention but did not compromise bone in growing swine

The Role of Tissues in the Anaerobic Metabolism of the Mussel Anodonta Hallenbeckii Lea

The participation of the carbonates of bone in the neutralization of ingested acid

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