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Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide
I T Demchenko1, A E Boso, P B Bennett
1Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Nitric Oxide : Biology and Chemistry
|January 5, 2001
Summary
Hyperbaric oxygen therapy reduces brain blood flow by decreasing nitric oxide (NO) availability and increasing reactive oxygen species (ROS). This study investigated the role of NO in hyperbaric oxygen-induced changes in cerebral blood flow.
Area of Science:
- Neuroscience
- Physiology
- Biochemistry
Background:
- Nitric oxide (NO) is implicated in hyperoxic vasoconstriction.
- Hyperbaric oxygen (HBO2) exposure can affect cerebral blood flow (CBF).
Purpose of the Study:
- To test the hypothesis that reduced NO availability in brain tissue during HBO2 exposure contributes to decreased regional cerebral blood flow (rCBF).
Main Methods:
- rCBF was measured in rats exposed to HBO2 at 5 atmospheres absolute (ATA).
- Brain levels of NO metabolites (NOx) and hydroxyl radical (•OH) were correlated with rCBF changes.
- Effects of NO synthase inhibitor (l-NAME), NO donor (PAPANONOate), and superoxide dismutase (MnSOD) were assessed during HBO2 exposure.
Main Results:
- HBO2 exposure (5 ATA) for 30 min decreased rCBF by 23-37% in several brain regions.
- Brain NOx levels decreased by 31% and correlated with reduced rCBF, while •OH production increased by 56%.
- MnSOD administration abolished the rCBF decrease, while NO donor had no effect during HBO2.
Conclusions:
- Decreased rCBF during HBO2 is associated with reduced effective NO concentration and increased reactive oxygen species (ROS) production in the brain.
- Inactivation of NO may antagonize basal cerebral vessel relaxation during HBO2 exposure.
- Further investigation into HBO2's effect on NO synthesis is warranted.
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