Brain carbonic acid acidosis after acetazolamide.
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.
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
D002255:Carbonic Acid; D000086:Acetazolamide; D011188:Potassium