Acid‐Base Changes in Rat Brain Tissue during Acute Respiratory Acidosis and Baseosis

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Abstract
The CO, buffer capacity of brain tissue in vivo was studied by measuring the tissue bicarbonate concentration at various tissue CO2 tensions in rats which were either hyperventilated, or breathed various CO2 concentrations spontaneously for 30 min. Measurements of the tissue lactate content indicated that the technique of freezing the tissue in situ did not lead to tissue hypoxia. The main increase in the tissue bicarbonate concentration at a given inspired CO2 concentration occurred within 30 min, but there was a slow further increase from 30 to 180 min. The values did not differ significantly between groups anesthetized with pentobarbital or phenobarbital and they were not influenced by variations of the inspired oxygen concentration from 20 to 50%. The mean tissue bicarbonate concentration was 16.0 meq/kg tissue H2O at a tissue CO2 tension (PtCO2) of 40 mm Hg. The buffer capacity of the tissue, defined as βCO2 = d log PtCO2/d log (HCO3/PtCO2 · S2) was 1.5. This means that when the CO2 tension was changed from 20 to 120 mm Hg, the tissue bicarbonate concentration increased from 12.5 to 22.5 meq/kg tissue H2O. Theoretical derivation of an equivalent buffer system with the same buffer capacity showed that at least 35 mmoles of buffer/kg tissue H2O were needed to explain the in vivo buffer capacity of the tissue. The theoretical buffer system made it possible to derive buffer base values for the tissue, and to construct a curve for the calculation of base excess values.