H+ transport from CNS in hypercapnia and regulation of CSF [HCO3-]

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Abstract
CSF HCO3- increases more than plasma HCO3- in hypercapnia, and there are at least 2 sources for the CSF HCO3- increase, one derived from the simultaneous increase in plasma HCO3-, and the other, HCO3- formed from hydration of CO2 in the choroid plexus and glia and susceptible to inhibition by acetazolamide. The H+ formed in the CNS in CO2 hydration may be actively exchanged from plasma Na+ utilizing the Na+-K+ ATPase pump. H+ transport from the CNS was studied in 4 groups of dogs breathing 5% CO2 at constant VA [rate of alveolar ventilation] for 4 h with repeated injections of saline, acetazolamide 5 mg/ml, ouabain 0.1 mg/ml and acetazolamide and ouabain together into lateral cerebral ventricles. Arterial HCO3- increased 2.5 meq/l at 4 h of hypercapnia in all groups. CSF HCO3- increased 5.8 meq/l in the saline-injected animals, but it increased only about 2 meq/l and equaled plasma HCO3- rise in the other 3 groups. Therefore CNS HCO3- formation in hypercapnia can be blocked by inhibiting the CO2 hydration reaction with acetazolamide or by blocking H+ removal by inhibiting Na+-K+ ATPase with ouabain. There may be active H+ removal from the CNS in exchange for plasma Na+ in hypercapnia.

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