engleski

The effect of acute hyperoxygenation on vascular relaxation mechanisms to ACh in Sprague-Dawley rats

Introduction: Results of our previous studies suggest that acute exposure to hyperbaric oxygen (HBO2) increases oxidative stress parameters (1). It is known that oxidative stress impairs vascular relaxation mechanisms in high dietary salt intake or hypertension. On the other hand, chronic, intermittent HBO2 exposure has beneficiary effect on vascular relaxation in diabetic animals (2). The synthesis of metabolites of arachidonic acid (AA) may be changed due to oxygen partial pressure alteration. Aim of this study was to examine the acute, single HBO2 exposure effects on the vascular reactivity to acetylcholine (ACh) in healthy male Sprague-Dawley rats. Methods: Fifty healthy Sprague-Dawley 9-12 weeks old rats were divided in two groups (25 rats per group) - control group and A-HBOT (acute HBO2 in a single 120 minutes session of 100% O2 at 2.0 bars with additionally 15 minutes for gradual compression and decompression). Response to ACh was studied in norepinephrine precontracted aortic rings (Isolated Organ Bath (Experimetria LTD) with or without L-NAME (NOS inhibitor), indomethacine (non-selective COX inhibitor, INDO), SOD mimetic TEMPOL or MS-PPOH (selective inhibitor of CYP450-epoxygenase that catalyses EETs production). Spectrophotometric method TBARS (Thiobarbituric Acid Reactive Substances) was used for measuring products of lipid peroxidation as a direct indicator of oxidative stress in arterial blood serum samples. Results: Acute exposure of healthy animals to HBO2 leads to the significantly impaired vasorelaxation response to ACh compared to control group. TEMPOL (10-5M) in vitro leads to recovery of vasorelaxation in response to ACh in A-HBOT group. In tested groups of rats, ACh induced vasorelaxation was mediated mainly by NO, with the contribution of CYP450 vasodilator metabolites in A-HBOT group respectively. Measuring of oxidative stress parameters (TBARS) showed significantly increased oxidative stress in A- HBOT group compared to control. Discussion: These results are in concordance with our previous study related to hyperbaric oxygenation. Increased oxidative stress in acute hyperbaric oxygen exposure and oxygen partial pressure changes were showed by Drenjancevic et.al 2013. Conclusion: Oxidative stress is increased in acute exposure to HBO2, which is probably the cause of dilation impairment. Hyperbaric oxygenation may lead to relaxation mechanism alteration mainly by activating CYP450 epoxygenation reactions and synthesis of EETs.

rat; hyperbaric oxygen therapy; vascular reactivity; oxidative stress

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