Fast bicarbonate-chloride exchange between brain cells and brain extracellular fluid in respiratory acidosis.

The extracellular pH, PCO2, and [Cl-] at the surface of the brain cortex, expiratory PCO2 and arterial blood pressure were continuously recorded in anaesthetized and artificially ventilated cats. The observations from such a preparation were: 1. In response to a nearly step increase in end-tidal PCO2, the brain ECF pH, PCO2, [Cl-] and calculated [HCO-3] changed in the form of a nearly mono-exponential time function after a delay of 5-7 s. 2. The time constants of the changes in the extracellular pH, PCO2, [Cl-] and [HCO-3] were in the range of 30-40 s. 3. The extracellular [HCO-3] increased markedly at an initial rate of 4.22 mmol.1(-1) . min-1 after 36 s. 4. This increase occurred almost simultaneously with a decrease in the extracellular [Cl-]. An [HCO-3]-[Cl-] exchange ratio was determined which very closely approached one. It is concluded that the brain extracellular bicarbonate concentration in respiratory acidosis increases because the H+ formed from the hydrated CO2 reacts with the intracellular buffers of brain cells, mainly glial cells, and HCO-3 inside the cell is formed and exchanged for Cl- outside the cell similar to the HCO-3/Cl- exchange which occurs between red cells and blood plasma during CO2 loading. The described time constants of the anion exchange represent the wash in or wash out time of CO2 in a tissue containing intracellular buffer.