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J L Gamble

Publications and source records attributed to J L Gamble.

13 recordsLinked to original sources
PubMed1982

Bicarbonate concentrations in the renal cortex.

Total CO2 (CO2+HCO3-) was measured in alkaline extracts of quickly frozen rat renal cortex. The mean concentration calculated for tissue water was 18.7 +/- SD 1.6 mEq/l (n = 10) when that measured in plasma water was 23.5 +/- 1.7. In other experiments (n = 6-10), the mean concentration in tissue water increased to 28.3 mEq/l after the animals were treated with benzolamide to inhibit carbonic anhydrase and to 38.1 mEq/l after they were infused with NaHCO3. On the other hand, the tissue concentration decreased to 14-15 mEq/l when they were hyperventilated or infused with HCl. Calculations based on published micropuncture data indicate that the usual intracellular concentration is 20-25 mEq/l or about twice that usually reported for skeletal muscle; and in contrast to muscle, the findings are suggestive of large variations in metabolic disorders.

Acidosis, Respiratory↗
PubMed1977

Acid-base relationships in the different body compartments: the basis for a simplified diagnostic approach.

Special characteristics of cellular buffering must be taken into account in order to describe accurately acid-base relationships in the whole body. In particular, tissues other than blood are able to neutralize mineral acid independent of changes in Pco(2) and hence independent of large changes in extra- and intracellular pH. Although mechanistic details remain to be clarified, relationships that describe this tissue buffering in quantitative terms are well established. In this report, emphasis is placed on quantitative relationships that stress the need for diagnostic interpretation derived from acid-base changes within the whole body rather than simply within the blood compartment. Theoreticalproblems with respect ot buffering mechanisms in various body compartments are reviewed and analyzed.

Acid-Base Equilibrium↗
PubMed1975

Skeletal buffering of acute metabolic acidosis.

Decreases in the sodium content of bone were measured to evaluate the role of this tissue in the buffering of acute metabolic acidosis. The bones of rats and dogs were labeled with radiosodium prior to the infusion of HCl, and changes in the radioactivity were used to indicate the loss of bone sodium. Significant reductions in the skeletal sodium occurred within the first 5 h of acidosis, and these losses can only be partially attributed to the hyponatremia accompanying the acid infusion. Decreases were greatest in the smaller bones of the rat; and, in the dog, the losses from flat bones exceeded those of the long bones. Only the rapidly exchangeable sodium of bone was involved in the changes due to acidosis. Soft tissue buffering may be more important initially; during 1.5-h experiments, the skeletal losses were small and could be ascribed almost entirely to the decrease in the amount of sodium contained in bone water. However, at the end of 5.0 h, the quantity of sodium released from the skeleton is sufficient to account for much of the tissue buffering.

Acid-Base Equilibrium↗