Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions

Abstract

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF “metabolic” acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.