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

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Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen. / Vorstrup, S; Henriksen, L; Paulson, O B.

In: The Journal of Clinical Investigation, Vol. 74, No. 5, 11.1984, p. 1634-9.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vorstrup, S, Henriksen, L & Paulson, OB 1984, 'Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen', The Journal of Clinical Investigation, vol. 74, no. 5, pp. 1634-9. https://doi.org/10.1172/JCI111579

APA

Vorstrup, S., Henriksen, L., & Paulson, O. B. (1984). Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen. The Journal of Clinical Investigation, 74(5), 1634-9. https://doi.org/10.1172/JCI111579

Vancouver

Vorstrup S, Henriksen L, Paulson OB. Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen. The Journal of Clinical Investigation. 1984 Nov;74(5):1634-9. https://doi.org/10.1172/JCI111579

Author

Vorstrup, S ; Henriksen, L ; Paulson, O B. / Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen. In: The Journal of Clinical Investigation. 1984 ; Vol. 74, No. 5. pp. 1634-9.

Bibtex

@article{b6633f83d8c744788b216a52147bb320,
title = "Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen",
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.",
keywords = "Acetazolamide/pharmacology, Blood Gas Analysis, Brain/metabolism, Cerebrovascular Circulation/drug effects, Humans, Hydrogen-Ion Concentration, Oxygen Consumption/drug effects",
author = "S Vorstrup and L Henriksen and Paulson, {O B}",
year = "1984",
month = nov,
doi = "10.1172/JCI111579",
language = "English",
volume = "74",
pages = "1634--9",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "American Society for Clinical Investigation",
number = "5",

}

RIS

TY - JOUR

T1 - Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen

AU - Vorstrup, S

AU - Henriksen, L

AU - Paulson, O B

PY - 1984/11

Y1 - 1984/11

N2 - 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.

AB - 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.

KW - Acetazolamide/pharmacology

KW - Blood Gas Analysis

KW - Brain/metabolism

KW - Cerebrovascular Circulation/drug effects

KW - Humans

KW - Hydrogen-Ion Concentration

KW - Oxygen Consumption/drug effects

U2 - 10.1172/JCI111579

DO - 10.1172/JCI111579

M3 - Journal article

C2 - 6501565

VL - 74

SP - 1634

EP - 1639

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 5

ER -

ID: 279594747