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

Abstract

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.