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

The extracellular pH,\(P_{CO_2 } \), and [Cl⁻] at the surface of the brain cortex, expiratory\(P_{CO_2 } \) 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\(P_{CO_2 } \), the brain ECF pH,\(P_{CO_2 } \), [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,\(P_{CO_2 } \), [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·l⁻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 thewash in orwash out time of CO₂ in a tissue containing intracellular buffer.