Regulation of the CSF pH in Acute and Sustained Respiratory Acidosis

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Abstract
In order to study the regulation of the cerebrospinal fluid pH during hypercapnia, plasma and CSF acid‐base parameters were measured in rats exposed to about 11% CO2 for periods varying from 5 min to 5 days. When combined with previously measured CSF‐plasma d.c. potential differences, the plasma and CSF pH values and bicarbonate concentrations could be used to calculate electrochemical potential differences (δμ) for H+ and HCO3‐ between CSF and plasma. Hypercapnia lead to a 20 mEq/kg increase in the CSF bicarbonate concentration, most of which occurred during the first 24 h. There was a somewhat larger [HCO3‐] increase in the CSF than in plasma water but in none of the compartments did the pH normalize. In acute hypercapnia (5–180 min) the calculated δμH+ and δμHCO3 values changed in a direction which would favor influx of HCO3‐a into the CSF. In the sustained groups (24–120h) the δμ's were close to the normocapnic control values. Since the accumulation of bicarbonate in the CSF occurred at a time when there was a suitable “passive” diffusion gradient, and since the CSF [HCO3‐] in the chronic state was upheld without a significant change in the δμ's, it is concluded that the regulation of the CSF pH in hypercapnia does not seem to require active transport of H+ or HCO3‐.

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