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

D. R. Gutsaeva, A. N. Moskvin, S. Yu Zhilyaev, V. B. Kostkin, I. T. Demchenko

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


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
Issue number7
StatePublished - Sep 2005
Externally publishedYes


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

ASJC Scopus subject areas

  • Neuroscience(all)


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