Abstract
The involvement of increased brain tissue CO2 tension in acetazolamide-induced brain acidosis was investigated by comparing the brain pH response to acetazolamide with that to hypercapnia. CO2 and pH sensors were placed bilaterally into cerebral white matter to 15 mm depth in cats. Group I cats (n = 9) breathed spontaneously, and in situ brain tissue PCO2 and pH (PbCO2 and pHb) were measured after intravenous acetazolamide administration (20 mg/kg). Group 2 cats (n = 9) were paralyzed and ventilated mechanically, and the changes of pHb were investigated by adjusting the ventilation to maintain the same Pbco2 values as in the acetazolamide-treated group. Pbco2 changes were not significantly different between the two groups. However, pHb responses were quite different: the fall in pHb was progressive in Group 1 but transient in Group 2. Brain acidosis after acetazolamide administration is not due to the rise in brain tissue CO2 tension.
