Brain and cerebrospinal fluid ionic composition and ventilation in acute hypercapnia

Rats were exposed to 11% CO2 in air for 15 min or 3 h and measurements made of ventilation, CSF acid-base values, and blood, CSF and brain electrolytes. Brain tissue HCO3- was studied by performing CO2 titration curves of tissue homogenates in vitro, the upward displacement of these curves reflecting the non-physico-chemical buffer mechanisms prominent in sustained hypercapnia. At 15 min, the CO2 induced increase in [HCO3-] was accompanied in CSF by an equimolar increase in [Na+] and in brain tissue by an increase in [K+]. At 3 h, the further increase in [HCO3-] was accompanied in CSF by a smaller increase in [Na+] and a decrease in [Cl-] and in brain tissue, there were no longer any significant changes in monovalent ions. In brain, the immediate pH regulatory response to hypercapnia appears to involve physico-chemical buffering and an ionic exchange with blood while by 3 h, the further increase in cell HCO3- must reflect altered cell metabolism. In CSF, the immediate increase in [Na+] and [HCO3-] is probably via choroid plexus while by 3 h, the CSF [HCO3-] increase could reflect exchange with blood at non-choroidal sites or to a less likely extent exchange with brain cells. CSF and brain cell pH regulation is reflected in ventilation which is lower at 3 h than at 15 min of CO2 exposure.