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J Appl Physiol 88: 1381-1389, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 4, 1381-1389, April 2000

Nitric oxide and cerebral blood flow responses to hyperbaric oxygen

Ivan T. Demchenko1, Albert E. Boso2, Thomas J. O'Neill2, Peter B. Bennett2, and Claude A. Piantadosi2

1 Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg 199034, Russia; and 2 The F. G. Hall Laboratory, Duke University Medical Center, Durham, North Carolina 27710

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O2 (HBO2) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O2 exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor (Nomega -nitro-L-arginine methyl ester), L-arginine, NO donors, or the N-methyl-D-aspartate receptor inhibitor MK-801. After 30 min of O2 exposure at 3 and 4 ATA, rCBF decreased by 26-39% and by 37-43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with Nomega -nitro-L-arginine methyl ester and exposed to HBO2 at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO2 at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO2, but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.

oxygen toxicity; glutamate neurotransmission; central nervous system


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