CONSECUTIVE ACID-BASE CHANGES IN BLOOD, BRAIN TISSUE AND CEREBROSPINAL FLUID DURING RESPIRATORY ACIDOSIS AND BASEOSIS

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Abstract
CO2 titration curves in vivo were determined simultaneously in arterial plasma, brain tissue and cisternal cerebrospinal fluid (CSF) of rats anaesthetized with pentobarbital and exposed to respiratory acidosis and baseosis for 15, 30, 60 or 180 min. The main changes in bicarbonate concentrations occurred within 15 min. in plasma ad brain tissue while there was a progressive increase in the CSF bicarbonate in hypercapnia and a decrease in hypocapnia. In hypercapnia (PaCO2 = 125 mm Hg)the increases in the bicarbonate concentration from control values (PaCO2 = 50 mm Hg) after 3 hr. were 6.6, 9.0 and 14.9 mEq/kg H2O in brain tissue, cerebral capillary plasma and CSF, respectively. In hypocapnia (PaCO2 = 18 mm Hg) there were corresponding decreases of the bicarbonate concentration in brain tissue water (2.1 mEq/kg) and in CSF (7.0 mEq/kg). However, there was a marked reduction of the plasma bicarbonate concentration with the Pa,CO2 in hypocapnia (PaCO2 [less than] 25 mm Hg) indicating a substantial accumulation of fixed acids at these low CO2 tensions. A CO2 titration curve for the intracellular water phase of the brain tissue was calculated assuming an extracellular space of 15% and an extracellular bicarbonate concentration equal to that of CSF. This calculation indicated that the buffer capacity of the intracellular phase was similar to that of while blood in vivo. The large bicarbonate changes in the CSF exclude the possibility that the CSF changes passively reflect blood or tissue buffering.