title: Brain carbonic acid acidosis after acetazolamide.
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: D000086:Acetazolamide / Q000008:administration & dosage; D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000139:chemically induced* / Q000378:metabolism; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D002255:Carbonic Acid / Q000494:pharmacology; D002415:Cats; D006863:Hydrogen-Ion Concentration; D007275:Injections, Intravenous; D011188:Potassium / Q000378:metabolism; D013997:Time Factors
chemical_list: D002255:Carbonic Acid; D000086:Acetazolamide; D011188:Potassium