Tissue and Renal Response to Chronic Respiratory

The elevation of pCO2 which occurs during respiratory acidosis is accompanied by a rise in the concentration of bicarbonate and a fall in the concentration of chloride in serum (1). The increased bicarbonate concentration results from both cellular and renal responses. The cellular response is characterized by the exchange of extracellular hydrogen ions for intracellular cations, thereby contributing to the elevation of the extracellular concentration of bicarbonate (2, 3). The renal factors responsible for the elevated bicarbonate concentration may be divided into two phases: 1) acid excretion, and 2) bicarbonate reabsorption. In acute human experiments, augmented acid excretion, as evidenced by increased excretion of ammonia and titratable acid, has been reported (4). Barker, Singer, Elkinton and Clark observed these changes also, but noted that if the urine was acid prior to breathing carbon dioxide, further increase in acid excretion may not occur (5). Perhaps this explains, in part at least, the failure of Longson and Mills to find increased acid excretion during short term human experiments (6). In acute respiratory acidosis tubular reabsorption of bicarbonate is increased (7). Moreover, in chronic respiratory acidosis in dogs, there is a further augmentation of reabsorption of bicarbonate that varies directly with the duration of the imposed acidosis (8). The fall in the concentration of serum chloride during respiratory acidosis may also result from both cellular and renal responses. The only cell into which chloride has been clearly demonstrated