Effects in man of acute experimental respiratory alkalosis and acidosis on ionic transfers in the total body fluids.

Although the concept of tissue buffering was formulated early in the study of acid-base disturbances, attention in the past has been directed primarily towards the effects of these disturbances on blood and extracellular fluid. More recently the demonstration by Darrow and his co-workers (1-3) of exchanges of intracellular cations during clinical and experimental potassium deficiency stimulated renewed interest in the quantitative aspects of the buffering action of intracellular fluid. Accordingly, some years ago the authors undertook quantitative estimation of the effects in man of acute experimental respiratory alkalosis and acidosis on the components of the multiphase system of red cells, plasma, interstitial fluid, and "intracellular" fluid (calculated as the non-chloride space), as well as on exchanges in the kidney. The latter renal effects will be reported in another paper (4). Our results indicate that in man the effects of acute hyperventilation or carbon dioxide inhalation are buffered to a large extent by a series of linked ionic exchanges with a phase or phases outside the chloride space, as well as with buffer systems within the blood and extracellular fluid. Since these findings were reported in abstract (5-8) similar conclusions have been reached by Giebisch, Berger, and Pitts (9), on the basis of experimental respiratory disturbances in the dog. Estimates of the importance of tissue buffering