The Regulation of Extra‐ and Intracellular Acid‐Base Parameters in the Rat Brain during Hyper‐ and Hypocapnia

Abstract

Abstract The influence of hyper‐ and hypocapnia upon extra‐ and intracellular acid‐base parameters in the brain was studied in rats anaesthetized with nitrous oxide. The arterial CO 2 tension was held constant at various values between 12 and 90 mm Hg for 45 min. Assuming a 12 per cent extracellular volume, the intracellular buffer capacity (β= d log Pco 2 /d pH) could be calculated to 2.27, the intracellular bicarbonate concentration to 14.3 meq/kg of cell water and the equivalent intracellular pH to 7.10 at a tissue C0 2 tension of 40 mm Hg. Between the tissue Pco 2 levels of 20 to 90 mm Hg the CSF bicarbonate varied by 19.5 meq/kg while the corresponding change in the intracellular bicarbonate concentration could be calculated to 12 meq/kg of intracellular water. The calculated buffer capacity of the CSF and intracellular phases greatly exceeded that of arterial blood in vivo . However, the buffering was not constant at different CO 2 tensions but increased at low C0 2 tensions to approach infinite buffering power at extreme hyperventilation. The varying buffer capacity indicates that pH in the extra‐ and intracellular spaces of the brain is regulated not only by physicochemical buffering but also by metabolic mechanisms. The results strongly suggest that the metabolic control is partly exerted by variations in the lactic acid production since the progressive increase in the calculated buffer capacity at low CO 2 tensions was parallelled by a continuously increasing lactate concentration, and since the constant buffer capacity at CO 2 tensions exceeding 50 mm Hg was associated with lactate concentrations which hardly varied at all.