Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition. / Gjedde, Albert; Johannsen, Peter; Cold, Georg; Østergaard, Leif.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 25, No. 9, 2005, p. 1183-96.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Gjedde, A, Johannsen, P, Cold, G & Østergaard, L 2005, 'Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition', Journal of Cerebral Blood Flow and Metabolism, vol. 25, no. 9, pp. 1183-96. https://doi.org/10.1038/sj.jcbfm.9600113

APA

Gjedde, A., Johannsen, P., Cold, G., & Østergaard, L. (2005). Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition. Journal of Cerebral Blood Flow and Metabolism, 25(9), 1183-96. https://doi.org/10.1038/sj.jcbfm.9600113

Vancouver

Gjedde A, Johannsen P, Cold G, Østergaard L. Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition. Journal of Cerebral Blood Flow and Metabolism. 2005;25(9):1183-96. https://doi.org/10.1038/sj.jcbfm.9600113

Author

Gjedde, Albert ; Johannsen, Peter ; Cold, Georg ; Østergaard, Leif. / Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition. In: Journal of Cerebral Blood Flow and Metabolism. 2005 ; Vol. 25, No. 9. pp. 1183-96.

Bibtex

@article{11300b60b31511debc73000ea68e967b,
title = "Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition",
abstract = "The reactions of cerebral metabolism to imposed changes of cerebral blood flow (CBF) are poorly understood. A common explanation of the mismatched CBF and oxygen consumption (CMR(O(2))) during neuronal excitation holds that blood flow rises more than oxygen consumption to compensate for an absent oxygen reserve in brain mitochondria. The claim conversely implies that oxygen consumption must decline when blood flow declines. As the prevailing rate of reaction of oxygen with cytochrome c oxidase is linked to the tension of oxygen, the claim fails to explain how oxygen consumption is maintained during moderate reductions of CBF imposed by hyperventilation (hypocapnia) or cyclooxygenase (COX) inhibition. To resolve this contradiction, we extended the previously published oxygen delivery model with a term allowing for the adjustment of the affinity of cytochrome c oxidase to a prevailing oxygen tension. The extended model predicted constant oxygen consumption at moderately reduced blood flow. We determined the change of affinity of cytochrome c oxidase in the extended model by measuring CBF in seven, and CMR(O(2)) in five, young healthy volunteers before and during COX inhibition with indomethacin. The average CBF declined 35%, while neither regional nor average CMR(O(2)) changed significantly. The adjustment of cytochrome c oxidase affinity to the declining oxygen delivery could be ascribed to a hypothetical factor with several properties in common with nitric oxide.",
author = "Albert Gjedde and Peter Johannsen and Georg Cold and Leif {\O}stergaard",
year = "2005",
doi = "10.1038/sj.jcbfm.9600113",
language = "English",
volume = "25",
pages = "1183--96",
journal = "Journal of Cerebral Blood Flow and Metabolism",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "9",

}

RIS

TY - JOUR

T1 - Cerebral metabolic response to low blood flow: possible role of cytochrome oxidase inhibition

AU - Gjedde, Albert

AU - Johannsen, Peter

AU - Cold, Georg

AU - Østergaard, Leif

PY - 2005

Y1 - 2005

N2 - The reactions of cerebral metabolism to imposed changes of cerebral blood flow (CBF) are poorly understood. A common explanation of the mismatched CBF and oxygen consumption (CMR(O(2))) during neuronal excitation holds that blood flow rises more than oxygen consumption to compensate for an absent oxygen reserve in brain mitochondria. The claim conversely implies that oxygen consumption must decline when blood flow declines. As the prevailing rate of reaction of oxygen with cytochrome c oxidase is linked to the tension of oxygen, the claim fails to explain how oxygen consumption is maintained during moderate reductions of CBF imposed by hyperventilation (hypocapnia) or cyclooxygenase (COX) inhibition. To resolve this contradiction, we extended the previously published oxygen delivery model with a term allowing for the adjustment of the affinity of cytochrome c oxidase to a prevailing oxygen tension. The extended model predicted constant oxygen consumption at moderately reduced blood flow. We determined the change of affinity of cytochrome c oxidase in the extended model by measuring CBF in seven, and CMR(O(2)) in five, young healthy volunteers before and during COX inhibition with indomethacin. The average CBF declined 35%, while neither regional nor average CMR(O(2)) changed significantly. The adjustment of cytochrome c oxidase affinity to the declining oxygen delivery could be ascribed to a hypothetical factor with several properties in common with nitric oxide.

AB - The reactions of cerebral metabolism to imposed changes of cerebral blood flow (CBF) are poorly understood. A common explanation of the mismatched CBF and oxygen consumption (CMR(O(2))) during neuronal excitation holds that blood flow rises more than oxygen consumption to compensate for an absent oxygen reserve in brain mitochondria. The claim conversely implies that oxygen consumption must decline when blood flow declines. As the prevailing rate of reaction of oxygen with cytochrome c oxidase is linked to the tension of oxygen, the claim fails to explain how oxygen consumption is maintained during moderate reductions of CBF imposed by hyperventilation (hypocapnia) or cyclooxygenase (COX) inhibition. To resolve this contradiction, we extended the previously published oxygen delivery model with a term allowing for the adjustment of the affinity of cytochrome c oxidase to a prevailing oxygen tension. The extended model predicted constant oxygen consumption at moderately reduced blood flow. We determined the change of affinity of cytochrome c oxidase in the extended model by measuring CBF in seven, and CMR(O(2)) in five, young healthy volunteers before and during COX inhibition with indomethacin. The average CBF declined 35%, while neither regional nor average CMR(O(2)) changed significantly. The adjustment of cytochrome c oxidase affinity to the declining oxygen delivery could be ascribed to a hypothetical factor with several properties in common with nitric oxide.

U2 - 10.1038/sj.jcbfm.9600113

DO - 10.1038/sj.jcbfm.9600113

M3 - Journal article

C2 - 15815583

VL - 25

SP - 1183

EP - 1196

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

SN - 0271-678X

IS - 9

ER -

ID: 14944108