Intracellular Acid-Base Regulation. II. The Interaction between CO2 Tension and Extracellular Bicarbonate in the Determination of Muscle Cell pH *

Abstract

A systematic study of the interaction between pH, PCO2, and external [HCO3-] in the regulation of muscle cell pH in an intact rat diaphragm preparation is presented. The results demonstrate that cell pH is a complex function, influenced by all three factors external pH, external [HCO3-], and pCO2. At any given external [HCO3-] cell pH could be changed by PCO2, and at any given pCO2 cell pH varied with external [HCO3]. At the same external pH, cell pH was dependent upon the absolute values of pCO2 and external [HCO3-]. CO2 tension had a relatively greater influence on cell pH than did extracellular [HCO3-]. Partial respiratory compensation of extracellular metabolic acidosis readily prevented cellular acidosis and even caused paradoxical cellular alkalosis, despite moderately low external pH. Partial compensatory rise in external [HCO3-] moderated but did not fully prevent cellular acidosis in severe hypercapnia. However, irrespective of absolute levels of pCO2 or external [HCO3-], whenever external pH fell below 6.85 the cell was acidotic. All degrees of extracellular alkalosis caused alkalinization of cells, regardless of compensatory changes in pCO2 or external [HCO3-]. The muscle cell was usually more acid than its environment, but became more alkaline when PCO2 was reduced in severe extracellular acidosis. Some clinical implications of these experiments are discussed. It is suggested that the regulation of the pH of resting skeletal muscle cannot be explained by simple buffer reactions and is probably linked to active metabolic processes.