Effects of acetazolamide and electrical stimulation on cerebral oxidative metabolism as indicated by the cytochrome oxidase redox state

The intravenous administration of acetazolamide to rats caused a prompt oxidation of cytochrome a,a₃ that was associated with an increase in the rate at which this cytochrome underwent additional oxidation and reductive recovery after electrical stimulation of the cerebral cortex. These effects were not observed in animals made hypercapnic after ventilation with 5% CO₂. The speed with which these and other metabolic and physiological events occur, after administering the drug, suggests that acetazolamide exerts its effects by complex mechanisms and that the site of action may be in the region of the blood-brain barrier, an area rich in carbonic anhydrase, and noradrenergic innervation.