Correction of CSF HCO-3 after its experimental increase in normocapnia: inhibition by acetazolamide.

In anaesthetized normocapnic dogs CSF [HCO-3] was increased to ca 33 mmol/l by perfusing the brain ventricles for 45 min with a mock CSF containing a high [HCO-3] which in addition contained 2.5 mg/ml acetazolamide to inhibit central carbonic anhydrase. In dogs with normal plasma [HCO-3], CSF [HCO-3] fell by 5.4 mmol/l in 2 h following the end of the perfusion. Lowering plasma [HCO-3] to 11 mmol/l by infusing HCl intravenously increased the CSF [HCO-3] fall to 7.5 mmol/l. Increasing plasma [HCO-3] to 36 mmol/l completely impeded the fall in CSF [HCO-3]. It is concluded that in these experiments clearing of HCO-3 from the CSF is critically dependent on plasma [HCO-3]. When the data are compared to those of comparable experiments without intraventricular administration of acetazolamide (Weyne et al. 1982), they indicate that acetazolamide impedes clearing of HCO-3 from CSF at high and at normal plasma [HCO-3] but not at low plasma [HCO-3]. The experiments therefore suggest a dual contribution for the clearing of HCO-3 from the CSF after its experimental increase: diffusion along the CSF-plasma gradient for HCO-3 and a carbonic anhydrase dependent clearing of HCO-3.