Abstract
The carbonic anhydrase inhibitor, acetazolamide (Maren, 1967), has been used clinically for many years as a treatment for the prevention of the symptoms, primarily headaches, of acute exposure to altitude hypoxia, as originally demonstrated by Cain and Dunn (1966). This effect was thought to be due to a drug-induced metabolic acidosis that compensated for an altitude-induced respiratory alkalosis. Furthermore, it had already been noticed that acetazolamide administration was followed by increased cerebral blood flow (Cotev et al., 1968; Ehrenreich et al., 1961; Posner and Plum, 1960), an observation that has often been confirmed since. Nevertheless, the effects of acetazolamide on metabolism and blood flow in the brain and their relationships to the physiological mechanisms of action of acetazolamide have not been well studied.
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© 1990 Plenum Press, New York
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LaManna, J.C., McCracken, K.A. (1990). Carbonic Anhydrase Inhibition and Cerebral Cortical Oxygenation in the Rat. In: Piiper, J., Goldstick, T.K., Meyer, M. (eds) Oxygen Transport to Tissue XII. Advances in Experimental Medicine and Biology, vol 277. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8181-5_39
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DOI: https://doi.org/10.1007/978-1-4684-8181-5_39
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