Acute Hyperbaric Oxygenation, Contrary to Intermittent Hyperbaric Oxygenation, Adversely Affects Vasorelaxation in...

The present study was aimed at assessing endothelium-dependent vasorelaxation, at measuring superoxide production in the aorta and femoral artery, and at determining antioxidative enzyme expression and activity in aortas of male Sprague-Dawley rats (N = 135), randomized to an A-HBO₂ group exposed to a single hyperbaric oxygenation session (120' of 100% O₂ at 2.0 bars), a 24H-HBO₂ group (single session, examined 24 h after exposure), a 4D-HBO₂ group (4 consecutive days of single sessions), and a CTRL group (untreated group). Vasorelaxation of aortic rings in response to acetylcholine (AChIR) and to reduced pO₂ (HIR) was tested in vitro in the absence/presence of NOS inhibitor L-NAME and superoxide scavenger TEMPOL. eNOS, iNOS, antioxidative enzyme, and NADPH oxidase mRNA expression was assessed by qPCR. Serum oxidative stress markers and enzyme activity were assessed by spectrometry, and superoxide production was determined by DHE fluorescence. Impaired AChIR and HIR in the A-HBO₂ group were restored by TEMPOL. L-NAME inhibited AChIR in all groups. Serum oxidative stress and superoxide production were increased in the A-HBO₂ group compared to all other groups. The mRNA expression of iNOS was decreased in the A-HBO₂ and 24H-HBO₂ groups while SOD1 and 3 and NADPH oxidase were increased in the 4D-HBO₂ group. The expression and activity of catalase and glutathione peroxidase were increased in the 4D-HBO₂ group as well. AChIR was NO dependent. Acute HBO₂ transiently impaired vasorelaxation due to increased oxidative stress. Vasorelaxation was restored and oxidative stress was normalized 24 h after the treatment.