Dogs were made alkalotic and hypochloremic by peritoneal dialysis using an isoosmotic, chloride-free, bicarbonate-rich solution. No potassium deficit was induced by the procedure. Following dialysis, the animals voided large quantities of bicarbonate, sodium, and potassium with partial correction of alkalosis. Subsequently chloride was restricted while sodium and potassium were given as phosphate or sulfate. Plasma bicarbonate rose by 4 mEq/liter while renal excretion of acid increased slightly above control values and sodium was retained. Upon readministration of chloride, retention of chloride and potassium was associated with prompt correction of alkalosis. Chloride space returned to control values while renal excretion of acid did not change. In two experiments, chloride replacement was undertaken during potassium restriction. Again prompt correction of alkalosis was observed while potassium deficit remained unchanged. Renal excretion of acid decreased moderately. The data suggest that the renal tubules are limited in their capacity to reabsorb bicarbonate following acute chloride depletion alkalosis. The administration of impermeant anions favors the maintenance and progression of alkalosis. In the absence of significant reduction in renal excretion of acid, re-expansion of extracellular compartment could be viewed as an important factor in the correction of alkalosis.
- metabolic alkalosis
- anions and metabolic alkalosis
- chloride depletion
- Copyright © 1964 by American Physiological Society