Hyperoxic Vasoconstriction in the Brain Is Mediated by Inactivation of Nitric Oxide by Superoxide Anions

S. Yu Zhilyaev; A. N. Moskvin; T. F. Platonova; D. R. Gutsaeva; I. V. Churilina; I. T. Demchenko

doi:10.1023/A:1025145331149

Hyperoxic Vasoconstriction in the Brain Is Mediated by Inactivation of Nitric Oxide by Superoxide Anions

S. Yu Zhilyaev, A. N. Moskvin, T. F. Platonova, D. R. Gutsaeva, I. V. Churilina, I. T. Demchenko

Research output: Contribution to journal › Article › peer-review

67 Scopus citations

Abstract

The hypothesis that decreases in brain blood flow during respiration of hyperbaric oxygen result from inactivation of nitric oxide (NO) by superoxide anions (O₂^-) is proposed. Changes in brain blood flow were assessed in conscious rats during respiration of atmospheric air or oxygen at a pressure of 4 atm after dismutation of O₂^- with superoxide dismutase or suppression of NO synthesis with the NO synthase inhibitor L-NAME. I.v. administration of superoxide dismutase increased brain blood flow in rats breathing air but was ineffective after previous inhibition of NO synthase. Hyperbaric oxygenation at 4 atm induced decreases in brain blood flow, though prior superoxide dismutase prevented hyperoxic vasoconstriction and increased brain blood flow in rats breathing hyperbaric oxygen. The vasodilatory effect of superoxide dismutase in hyperbaric oxygenation was not seen in animals given prior doses of the NO synthase inhibitor. These results provide evidence that one mechanism for hyperoxic vasoconstriction in the brain consists of inactivation of NO by superoxide anions, decreasing its basal vasorelaxing action.

Original language	English (US)
Pages (from-to)	783-787
Number of pages	5
Journal	Neuroscience and Behavioral Physiology
Volume	33
Issue number	8
DOIs	https://doi.org/10.1023/A:1025145331149
State	Published - Oct 2003
Externally published	Yes

Keywords

Brain blood flow
Hyperbaric oxygenation
Nitric oxide
Superoxide anion
Superoxide dismutase

ASJC Scopus subject areas

General Neuroscience

Access to Document

10.1023/A:1025145331149

Cite this

@article{a759d5da024547fc8539e3a53a45dd28,

title = "Hyperoxic Vasoconstriction in the Brain Is Mediated by Inactivation of Nitric Oxide by Superoxide Anions",

abstract = "The hypothesis that decreases in brain blood flow during respiration of hyperbaric oxygen result from inactivation of nitric oxide (NO) by superoxide anions (O2-) is proposed. Changes in brain blood flow were assessed in conscious rats during respiration of atmospheric air or oxygen at a pressure of 4 atm after dismutation of O2- with superoxide dismutase or suppression of NO synthesis with the NO synthase inhibitor L-NAME. I.v. administration of superoxide dismutase increased brain blood flow in rats breathing air but was ineffective after previous inhibition of NO synthase. Hyperbaric oxygenation at 4 atm induced decreases in brain blood flow, though prior superoxide dismutase prevented hyperoxic vasoconstriction and increased brain blood flow in rats breathing hyperbaric oxygen. The vasodilatory effect of superoxide dismutase in hyperbaric oxygenation was not seen in animals given prior doses of the NO synthase inhibitor. These results provide evidence that one mechanism for hyperoxic vasoconstriction in the brain consists of inactivation of NO by superoxide anions, decreasing its basal vasorelaxing action.",

keywords = "Brain blood flow, Hyperbaric oxygenation, Nitric oxide, Superoxide anion, Superoxide dismutase",

author = "Zhilyaev, {S. Yu} and Moskvin, {A. N.} and Platonova, {T. F.} and Gutsaeva, {D. R.} and Churilina, {I. V.} and Demchenko, {I. T.}",

note = "Funding Information: This study was supported by the Russian Fund for Basic Research (Grant No. 00-04-49492).",

year = "2003",

month = oct,

doi = "10.1023/A:1025145331149",

language = "English (US)",

volume = "33",

pages = "783--787",

journal = "Neuroscience and Behavioral Physiology",

issn = "0097-0549",

publisher = "Springer New York",

number = "8",

}

TY - JOUR

T1 - Hyperoxic Vasoconstriction in the Brain Is Mediated by Inactivation of Nitric Oxide by Superoxide Anions

AU - Zhilyaev, S. Yu

AU - Moskvin, A. N.

AU - Platonova, T. F.

AU - Gutsaeva, D. R.

AU - Churilina, I. V.

AU - Demchenko, I. T.

N1 - Funding Information: This study was supported by the Russian Fund for Basic Research (Grant No. 00-04-49492).

PY - 2003/10

Y1 - 2003/10

N2 - The hypothesis that decreases in brain blood flow during respiration of hyperbaric oxygen result from inactivation of nitric oxide (NO) by superoxide anions (O2-) is proposed. Changes in brain blood flow were assessed in conscious rats during respiration of atmospheric air or oxygen at a pressure of 4 atm after dismutation of O2- with superoxide dismutase or suppression of NO synthesis with the NO synthase inhibitor L-NAME. I.v. administration of superoxide dismutase increased brain blood flow in rats breathing air but was ineffective after previous inhibition of NO synthase. Hyperbaric oxygenation at 4 atm induced decreases in brain blood flow, though prior superoxide dismutase prevented hyperoxic vasoconstriction and increased brain blood flow in rats breathing hyperbaric oxygen. The vasodilatory effect of superoxide dismutase in hyperbaric oxygenation was not seen in animals given prior doses of the NO synthase inhibitor. These results provide evidence that one mechanism for hyperoxic vasoconstriction in the brain consists of inactivation of NO by superoxide anions, decreasing its basal vasorelaxing action.

AB - The hypothesis that decreases in brain blood flow during respiration of hyperbaric oxygen result from inactivation of nitric oxide (NO) by superoxide anions (O2-) is proposed. Changes in brain blood flow were assessed in conscious rats during respiration of atmospheric air or oxygen at a pressure of 4 atm after dismutation of O2- with superoxide dismutase or suppression of NO synthesis with the NO synthase inhibitor L-NAME. I.v. administration of superoxide dismutase increased brain blood flow in rats breathing air but was ineffective after previous inhibition of NO synthase. Hyperbaric oxygenation at 4 atm induced decreases in brain blood flow, though prior superoxide dismutase prevented hyperoxic vasoconstriction and increased brain blood flow in rats breathing hyperbaric oxygen. The vasodilatory effect of superoxide dismutase in hyperbaric oxygenation was not seen in animals given prior doses of the NO synthase inhibitor. These results provide evidence that one mechanism for hyperoxic vasoconstriction in the brain consists of inactivation of NO by superoxide anions, decreasing its basal vasorelaxing action.

KW - Brain blood flow

KW - Hyperbaric oxygenation

KW - Nitric oxide

KW - Superoxide anion

KW - Superoxide dismutase

UR - http://www.scopus.com/inward/record.url?scp=1642482756&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642482756&partnerID=8YFLogxK

U2 - 10.1023/A:1025145331149

DO - 10.1023/A:1025145331149

M3 - Article

C2 - 14635993

AN - SCOPUS:1642482756

SN - 0097-0549

VL - 33

SP - 783

EP - 787

JO - Neuroscience and Behavioral Physiology

JF - Neuroscience and Behavioral Physiology

IS - 8

ER -

Hyperoxic Vasoconstriction in the Brain Is Mediated by Inactivation of Nitric Oxide by Superoxide Anions

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this