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Research Article Free access | 10.1172/JCI111579

Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen.

S Vorstrup, L Henriksen, and O B Paulson

Find articles by Vorstrup, S. in: JCI | PubMed | Google Scholar

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Published November 1, 1984 - More info

Published in Volume 74, Issue 5 on November 1, 1984
J Clin Invest. 1984;74(5):1634–1639. https://doi.org/10.1172/JCI111579.
© 1984 The American Society for Clinical Investigation
Published November 1, 1984 - Version history
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Abstract

The aim of this study was to evaluate the effect of acetazolamide on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). CBF, arterial and jugular venous partial O2 pressure, partial CO2 pressure, pH, and O2 saturation percentage were measured in six patients before and 3 and 20 minutes after intravenous administration of 1 g of acetazolamide. CBF was measured by the intracarotid 133xenon injection technique. In addition, changes in CBF were estimated from the arteriovenous oxygen content difference. CBF increased in all patients after acetazolamide, by approximately 55 and 70% after 3 and 20 min, respectively. The CBF changes were of the same order whether calculated from the 133Xe clearance or from the arteriovenous oxygen differences (A-V)O2. CMRO2, calculated from (A-V)O2 differences and CBF, remained constant. Except for an increase in the venous oxygen saturation, the blood gases remained constant. Acetazolamide, in a dose sufficient to inhibit the erythrocyte carbonic anhydrase (EC 4.2.1.1), thus induced a rapid and marked increase in CBF, leaving CMRO2 unchanged. This effect of acetazolamide on CBF is probably explained by a decrease in brain pH rather than by brain tissue hypoxia due to inhibition of oxygen unloading in the brain capillaries.

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