The Effect of Iso‐Carbic Metabolic Acidosis in Blood on [H+] and [HCO3‐] in CSF with Deductions about the Regulation of an Active Transport of H+/HCO3 ‐ between Blood and CSF

Abstract The changes in pH and [HCO3] in csf of anesthetized, paralyzed dogs during metabolic acidosis were compared with those changes when the blood acid‐base parameters were tept at a normal level. Arterial and csf Pco2 were kept constant at the same level during both kinds of experiments. Arterial [HCO3‐‐] was kept cmstant at about 25 meq/l during normal acid‐base experiments and at about 19 meq/l during acidosis experiments. Arterial and csf samples were simultaneously withdrawn after 1 hr, 3 hrs, and 6 hrs. The changes in csf pH and [HCO3‐‐] were expressed as the changes in the electrochemical potential differences (csf‐blood) for H+‘ and HCO3‐ During metabolic acidosis the electrochemical potential differences for H+ and HCO3‐ decreased which could be explained by a decrease in the rate of an active transport of H+/HCO3‐‐ between blood and csf during metabolic acidosis at a constant Pco2. The findings are compared with previous findings and we conclude that the rate of active transport of H+/HCO3‐ between blood and csf if affected by changes in plasma [HCO3‐]. This mechanism provides pH stability in the brain environment during metabolic blood acid‐base changes, whereas the effect is opposite during respiratory acid‐base changes. The mechanism is however “useful” during respiratory acidosis because it provides a negative feed‐back mechanism for the increase in Pco2 during respiratory acidosis.