Brain carbonic acid acidosis after acetazolamide

Acta Physiol Scand. 1975 Mar;93(3):385-90. doi: 10.1111/j.1748-1716.1975.tb05827.x.

Abstract

In cats in barbiturate anesthesia extracellular pH and potassium were continously recorded from brian cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood-brain-barrier to HCO3-minus and H+ions as indicated by the development of brain acidosis by I.V. injection of HCO3-minus. Acetazolamide (25 mg/kg) i.v. was followed by a marked brain acidosis which after 10 min had progressed to a drop in pH of 0.203 plus or minus 0.046 (x bar plus or minus S.D., n equals 8). The slowness ofthe development of acidosis points to a direct effect of the carbonic anhydrase inhibition on the brain tissue. As a further support for this conclusion was considered the finding of a prolonged response time of brain pH to HCO3-minus i.v. to CO2-minus inhalation, and to hyperventilation after the acetazolamide inhibtion. No changes in brain extracelllular potassium were found.

MeSH terms

  • Acetazolamide* / administration & dosage
  • Acid-Base Equilibrium
  • Acidosis / chemically induced*
  • Acidosis / metabolism
  • Animals
  • Blood-Brain Barrier
  • Brain / metabolism*
  • Carbonic Acid / pharmacology
  • Cats
  • Hydrogen-Ion Concentration
  • Injections, Intravenous
  • Potassium / metabolism
  • Time Factors

Substances

  • Carbonic Acid
  • Acetazolamide
  • Potassium