Evidence for a Carrier Mediated Exchange Diffusion of HCO 3 − Against Cl− at the Interphases of the Central Nervous System

Abstract

The kinetics of the in vivo CO2 dissociation curve of the brain extracellular fluid (ECF) revealed that as soon as the extracellular PCO2 was increased, there was a marked and instantaneous increase in the extracellular bicarbonate concentration (Ahmad et al. 1978). Further experiments were designed to find out if there was a counter exchange of HCO 3 − against Cl− at the interphase of the CNS. In these experiments brain ECF pH, pCO2, Cl−, and HCO 3 − changed, following closely mono-exponential time function after a delay of 5–7 s in response to a nearly step increase of end-tidal PCO2 in artificially ventilated cats. The most important observation from such a preparation was an increase of the extracellular HCO 3 − accompanied by a decrease of Cl− with a ratio of almost one to one and a time constant of 30 s. A similar rapid HCO 3 − -Cl− exchange has been shown to occur at the blood-brain ECF-barrier in metabolic disturbances while keeping paCO2 constant (Loeschcke and Ahmad, 1980, Ahmad and Loeschcke, 1982). These investigations led to a new concept regarding the exchange process of HCO 3 − and Cl− between blood plasma and the brain ECF on the one hand and between brain cells and the ECF on the other hand. Since the glial cells provide the bulk of the cell mass, they are the first candidates for the anion exchange. In respiratory acidosis such anion exchange is the leading process because CO2 from blood enters the extracellular fluid and the brain cells without restrictions then it reacts with intracellular buffers forming HCO 3 − which in turn is exchanged against Cl−. What is the mechanism of such a HCO 3 − - Cl− exchange in glial cells under the influence of their high membrane potential?