Abstract
Studies on conscious rats with inhibition of NO synthase were used to assess the dynamics of brain blood flow and EEG traces during hyperbaric oxygenation at 4 or 5 atm. Oxygen at a pressure of 4 atm induced cerebral vasoconstriction in intact animals and decreased blood flow by 11–18% (p < 0.05) during 60-min exposure to hyperbaric oxygenation. Paroxysmal EEG activity and oxygen convulsions did not occur in rats at 4 atm of O2. At 5 atm, convulsive activity appeared on the EEG at 41 ± 1.9 min, and blood flow decreased significantly during the first 20 min; blood flow increased by 23 ± 9%, as compared with controls, (p < 0.01) before the appearance of convulsions on the EEG. Prior inhibition of NO synthase I (NOS I) and NO synthase III (NOS III) with Nω-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) or inhibition only of NOS I with 7-nitroindazole (7-NI, 50 mg/kg) prevented the development of hyperoxic hyperemia and paroxysmal spikes on the EEG during hyperbaric oxygenation at 5 atm. These results show that hyperbaric oxygen induces changes in cerebral blood flow which modulate its neurotoxic action via nitric oxide synthesized both in neurons and in cerebral vessels.
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Moskvin, A.N., Zhilyaev, S.Y., Sharapov, O.I. et al. Brain Blood Flow Modulates the Neurotoxic Action of Hyperbaric Oxygen via Neuronal and Endothelial Nitric Oxide. Neurosci Behav Physiol 33, 883–888 (2003). https://doi.org/10.1023/A:1025996721736
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DOI: https://doi.org/10.1023/A:1025996721736