Acetazolamide and cerebral oxygenation in dogs

Acetazolamide could theoretically impair oxygen delivery to cerebral tissue by inhibiting local acidification of capillary blood. There is considerable evidence, however, that acetazolamide improves cerebral oxygen tension. This experiment was designed to demonstrate increased deep cerebral oxygen tension after acetazolamide. Three groups of dogs were anesthetized with pentobarbital and ventilated with a respirator. A Teflon-coated stainless steel catheter was placed through a craniotomy into the parietal lobe and advanced into the corona radiata to monitor cerebral pO2 and pCO2 with a mass spectrometer. Group one dogs were normoxic and eucapneic. Group two dogs were hypoxemic, and Group three dogs were hypocapneic. After control cerebral and arterial gas tensions had been recorded, acetazolamide (30 mg kg-1) was injected intravenously. Cerebral gas tensions were monitored continuously and arterial gases were analyzed at 30, 60, 90 and 120 min. Cerebral oxygen tension was not decreased by acetazolamide in any of the dogs. Cerebral carbon dioxide tension was increased by acetazolamide in all dogs. We conclude that acetazolamide does not deplete cerebral oxygen tension even in the face of hypoxemia or acute hypocapnea.