The Effects of Acetazolamide on Cerebral Blood Flow and Cerebral Tissue Po2

An experiment was designed to rule out bypoxia of cerebral tissue as a mediator of increased cerebral blood flow (CBF) due to acetazolamide (Diamox). Hypoxia might be produced by carbonic anhydrase inhibition by delaying the acidification of the red blood cell until it left the tissue capillary. Fifteen dogs were studied under pentobarbital anesthesia. CBF was estimated from the arteriovenous oxygen content difference across the brain. Cerebral tissue oxygen tension (Paco2) was measured directly on the cortical surface. CBF was altered by altering arterial Pco2 (Paco2) before and after the intravenous administration of 25 mg./kg. acetazolamide. At Paco2 = 30 mm. Hg, acetazolamide increased CBF by 69 per cent; at Paco2 = 40 mm. Hg, by 64 per cent; at Paco2 = 50 mm. Hg, by 55 per cent. This was accompanied by an increase in Po2 of 20 mm. Hg at Paco2 = 30 mm. Hg; 19 mm. Hg at Paco2 = 40 mm. Hg; 16 mm. Hg at Paco2 = 50 mm. Hg. Since Po2 increased, clinical use of the drug in association with mechanical ventilation in the treatment of chronic hypereapnia appears justified. The effect of acetazolamide on cerebrovascular tone remains unexplained.