Effects of Chronic Hypercapnia on Electrolyte

Previous studies have characterized the changes in acid-base equilibrium in dogs exposed over a prolonged period to a 12 per cent carbon dioxide atmosphere (1). Plasma bicarbonate concentration rose in a gradual curvilinear fashion over several days and became stabilized at maximal levels of 35 to 38 mEq per L. This adaptive response was not influenced by the level of sodium chloride intake. After the return of the dogs to room air, however, plasma bicarbonate concentration remained significantly elevated in dogs ingesting a low-salt diet. The resulting alkalosis persisted until chloride was provided, and then normal acidbase equilibrium was rapidly restored (2). During hypercapnia, the urine remained almost free of bicarbonate and it was therefore not possible to define fully the effects of hypercapnia on the mechanism for bicarbonate reabsorption; the capacity to reabsorb completely as much as 38 mEq of bicarbonate per L of filtrate may have been rapidly engendered by hypercapnia, but not fully employed for several days because of slow renal generation of bicarbonate. In order to evaluate further the effect of a high carbon dioxide tension on the renal threshold for bicarbonate, observations have been carried out in dogs whose diets were supplemented with large quantities of sodium bicarbonate. Under these circumstances, the rise in plasma bicarbonate concentration ought not to be limited by renal ability to generate bicarbonate, but rather by renal reabsorptive capacity. Observations have also been carried out