The roles of nitric oxide and carbon dioxide gas in the neurotoxic actions of oxygen under pressure

Diana Raisovna Gutsaeva, A. N. Moskvin, S. Yu Zhilyaev, V. B. Kostkin, I. T. Demchenko

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The hypothesis that in conditions of hyperbaric oxygenation, nitric oxide (NO) modulates the vasodilatory effect of CO2 in the brain and thus accelerates the neurotoxic action of oxygen was verified experimentally. Conscious rats breathed atmospheric air or oxygen at 5 atm and blood flow in the striatum was measured before and after inhibition of carbonic anhydrase with acetazolamide, which causes retention of CO2 in the brain. Acetazolamide (35 mg/kg) increased blood flow in the animals when breathing air by 38 ± 7.4% (p < 0.01), while preliminary inhibition of NO synthase with Nω-nitro-L-arginine-methyl ester (L-NAME, 30 mg/kg) significantly weakened its vasodilatory action. Inhibition of carbonic anhydrase in animals breathing hyperbaric oxygen at 5 atm prevented cerebral vasoconstriction, increased brain blood flow, and accelerated the development of oxygen convulsions. The vasodilatory effect of acetazolamide in hyperbaric oxygenation was significantly reduced in animals pretreated with the NO synthase inhibitor, such that the latent period of convulsions increased. The results obtained here provide evidence that in conditions of extreme hyperoxia, NO modulates the cerebral hyperemia developing in conditions of CO2 retention in the brain and accelerates the development of the neurotoxic actions of hyperbaric oxygen.

Original languageEnglish (US)
Pages (from-to)751-756
Number of pages6
JournalNeuroscience and Behavioral Physiology
Volume35
Issue number7
DOIs
StatePublished - Sep 1 2005
Externally publishedYes

Fingerprint

Carbon Dioxide
Nitric Oxide
Gases
Acetazolamide
Oxygen
Pressure
Hyperbaric Oxygenation
Carbonic Anhydrases
Brain
Nitric Oxide Synthase
Respiration
Seizures
Air
Hyperoxia
NG-Nitroarginine Methyl Ester
Hyperemia
Vasoconstriction

Keywords

  • Acetazolamide
  • Cerebral blood flow
  • Hyperbaric oxygenation
  • Nitric oxide
  • Oxygen convulsions

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

The roles of nitric oxide and carbon dioxide gas in the neurotoxic actions of oxygen under pressure. / Gutsaeva, Diana Raisovna; Moskvin, A. N.; Zhilyaev, S. Yu; Kostkin, V. B.; Demchenko, I. T.

In: Neuroscience and Behavioral Physiology, Vol. 35, No. 7, 01.09.2005, p. 751-756.

Research output: Contribution to journalArticle

Gutsaeva, Diana Raisovna ; Moskvin, A. N. ; Zhilyaev, S. Yu ; Kostkin, V. B. ; Demchenko, I. T. / The roles of nitric oxide and carbon dioxide gas in the neurotoxic actions of oxygen under pressure. In: Neuroscience and Behavioral Physiology. 2005 ; Vol. 35, No. 7. pp. 751-756.
@article{eaf6873892d2465a9e5c6dac1722f13f,
title = "The roles of nitric oxide and carbon dioxide gas in the neurotoxic actions of oxygen under pressure",
abstract = "The hypothesis that in conditions of hyperbaric oxygenation, nitric oxide (NO) modulates the vasodilatory effect of CO2 in the brain and thus accelerates the neurotoxic action of oxygen was verified experimentally. Conscious rats breathed atmospheric air or oxygen at 5 atm and blood flow in the striatum was measured before and after inhibition of carbonic anhydrase with acetazolamide, which causes retention of CO2 in the brain. Acetazolamide (35 mg/kg) increased blood flow in the animals when breathing air by 38 ± 7.4{\%} (p < 0.01), while preliminary inhibition of NO synthase with Nω-nitro-L-arginine-methyl ester (L-NAME, 30 mg/kg) significantly weakened its vasodilatory action. Inhibition of carbonic anhydrase in animals breathing hyperbaric oxygen at 5 atm prevented cerebral vasoconstriction, increased brain blood flow, and accelerated the development of oxygen convulsions. The vasodilatory effect of acetazolamide in hyperbaric oxygenation was significantly reduced in animals pretreated with the NO synthase inhibitor, such that the latent period of convulsions increased. The results obtained here provide evidence that in conditions of extreme hyperoxia, NO modulates the cerebral hyperemia developing in conditions of CO2 retention in the brain and accelerates the development of the neurotoxic actions of hyperbaric oxygen.",
keywords = "Acetazolamide, Cerebral blood flow, Hyperbaric oxygenation, Nitric oxide, Oxygen convulsions",
author = "Gutsaeva, {Diana Raisovna} and Moskvin, {A. N.} and Zhilyaev, {S. Yu} and Kostkin, {V. B.} and Demchenko, {I. T.}",
year = "2005",
month = "9",
day = "1",
doi = "10.1007/s11055-005-0119-9",
language = "English (US)",
volume = "35",
pages = "751--756",
journal = "Neuroscience and Behavioral Physiology",
issn = "0097-0549",
publisher = "Springer New York",
number = "7",

}

TY - JOUR

T1 - The roles of nitric oxide and carbon dioxide gas in the neurotoxic actions of oxygen under pressure

AU - Gutsaeva, Diana Raisovna

AU - Moskvin, A. N.

AU - Zhilyaev, S. Yu

AU - Kostkin, V. B.

AU - Demchenko, I. T.

PY - 2005/9/1

Y1 - 2005/9/1

N2 - The hypothesis that in conditions of hyperbaric oxygenation, nitric oxide (NO) modulates the vasodilatory effect of CO2 in the brain and thus accelerates the neurotoxic action of oxygen was verified experimentally. Conscious rats breathed atmospheric air or oxygen at 5 atm and blood flow in the striatum was measured before and after inhibition of carbonic anhydrase with acetazolamide, which causes retention of CO2 in the brain. Acetazolamide (35 mg/kg) increased blood flow in the animals when breathing air by 38 ± 7.4% (p < 0.01), while preliminary inhibition of NO synthase with Nω-nitro-L-arginine-methyl ester (L-NAME, 30 mg/kg) significantly weakened its vasodilatory action. Inhibition of carbonic anhydrase in animals breathing hyperbaric oxygen at 5 atm prevented cerebral vasoconstriction, increased brain blood flow, and accelerated the development of oxygen convulsions. The vasodilatory effect of acetazolamide in hyperbaric oxygenation was significantly reduced in animals pretreated with the NO synthase inhibitor, such that the latent period of convulsions increased. The results obtained here provide evidence that in conditions of extreme hyperoxia, NO modulates the cerebral hyperemia developing in conditions of CO2 retention in the brain and accelerates the development of the neurotoxic actions of hyperbaric oxygen.

AB - The hypothesis that in conditions of hyperbaric oxygenation, nitric oxide (NO) modulates the vasodilatory effect of CO2 in the brain and thus accelerates the neurotoxic action of oxygen was verified experimentally. Conscious rats breathed atmospheric air or oxygen at 5 atm and blood flow in the striatum was measured before and after inhibition of carbonic anhydrase with acetazolamide, which causes retention of CO2 in the brain. Acetazolamide (35 mg/kg) increased blood flow in the animals when breathing air by 38 ± 7.4% (p < 0.01), while preliminary inhibition of NO synthase with Nω-nitro-L-arginine-methyl ester (L-NAME, 30 mg/kg) significantly weakened its vasodilatory action. Inhibition of carbonic anhydrase in animals breathing hyperbaric oxygen at 5 atm prevented cerebral vasoconstriction, increased brain blood flow, and accelerated the development of oxygen convulsions. The vasodilatory effect of acetazolamide in hyperbaric oxygenation was significantly reduced in animals pretreated with the NO synthase inhibitor, such that the latent period of convulsions increased. The results obtained here provide evidence that in conditions of extreme hyperoxia, NO modulates the cerebral hyperemia developing in conditions of CO2 retention in the brain and accelerates the development of the neurotoxic actions of hyperbaric oxygen.

KW - Acetazolamide

KW - Cerebral blood flow

KW - Hyperbaric oxygenation

KW - Nitric oxide

KW - Oxygen convulsions

UR - http://www.scopus.com/inward/record.url?scp=23644454050&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=23644454050&partnerID=8YFLogxK

U2 - 10.1007/s11055-005-0119-9

DO - 10.1007/s11055-005-0119-9

M3 - Article

VL - 35

SP - 751

EP - 756

JO - Neuroscience and Behavioral Physiology

JF - Neuroscience and Behavioral Physiology

SN - 0097-0549

IS - 7

ER -