Acute Hyperbaric Oxygenation, Contrary to Intermittent Hyperbaric Oxygenation, Adversely Affects Vasorelaxation in Healthy Sprague‐Dawley Rats due to Increased Oxidative Stress

Abstract

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.

Arachidonic Acid Metabolites of CYP450 Enzymes and HIF-1α Modulate Endothelium-Dependent Vasorelaxation in Sprague-Dawley Rats under Acute and Intermittent Hyperbaric Oxygenation

“…The observed decrease in mean arterial pressure is consistent with our previous studies, which discuss this issue [ 18 , 29 ]. Oxidative stress induced impaired baseline AChIR and HIR in the A-HBO 2 group, which was also previously described and discussed in our previous study [ 18 ].…”

“…However, independently of hypoxic or normoxic conditions, free radicals are needed to express HIF-α [ 36 , 37 ]. In acute HBO 2 exposure, the oxidative stress is increased [ 18 ]. Previously, it has been shown that HIF-1 and -2 levels are increased in HBO 2 treatment due to increased ROS production [ 37 , 38 ].…”

“…Recently, we showed that increased superoxide production and an overall increase in oxidative stress impairs vasorelaxation in rats acutely exposed to HBO 2 , whereas intermittent exposure to HBO 2 increases the expression and activity of antioxidative enzymes, suggesting that intermittent HBO 2 induces antioxidative defense mechanisms underlying restored vasorelaxation [ 18 ]. Altogether, there is no clear answer as to which mediators are involved in the vasoconstriction or vasorelaxation observed in various HBO 2 protocols, because up to the present study, no measurements of vascular eicosanoids production have yet been performed.…”

Hyperbaric oxygen preconditioning and the role of NADPH oxidase inhibition in postischemic acute kidney injury induced in spontaneously hypertensive rats

“…In traumatic brain injury, HBO attenuates inflammatory responses by limiting production of inflammatory mediators, creating better environment for repair and regeneration [12]. However, these effects are dependent on treatment parameters-pressure and duration on the treatment [15,16].…”

Magnitude and Clinical Predictors of Blood Pressure Changes in Patients Undergoing Hyperbaric Oxygen Therapy: A Retrospective Study

“…This trend was more evident between patients with a history of hypertension compared to normotensive patients ( Figure 2 ); it is likely that the vasoconstrictive response becomes more pronounced after treatment, and it may either represent an improved arteriolar smooth muscle activity or a lack of vasorelaxation. While it has been described that repetitive HBOT improves the vasorelaxation [ 22 , 23 , 24 ], increased vascular stiffness might play a role in impairing this response in patients with a history of hypertension.…”