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INTRODUCTION: Diabetes mellitus leads to impaired endothelial function. Clinical studies established beneficial role of hyperbaric oxygen therapy in diabetic wound healing, however, the mechanisms are not clearly defined. The aim of this study was to determine the effect of intermittent hyperbaric oxygenation (HBOT) on vascular responses to reduced pO2 in diabetic rats. METHODS:Prior to experiments, rats were anesthetized with ketamin (75 mg/kg) and midazolam (2.5 mg/kg) i.p. Isolated middle cerebral arteries (MCA) of male control, diabetic DM (streptozocin 60mg/kg i.p.) and HBOT treated diabetic rats (DM+HBOT) Sprague-Dawley rats (N=10 per group) were mounted on glass pipettes of DMT 110P pressure myograph system for internal diameter measurements in normoxia (21% O2 in superfusate and perfusate, and reduced pO2 (0%) condition. HBOT rats were treated in a hyperbaric chamber with 100% O2 (2 bar) 2 hours/day for 4 consecutive days. To assess the role of CYP450- epoxygenases' vasodilating metabolites (EETs), the CYP450 inhibitor - clotrimazole was used. The role of KATP channels in hypoxic response was assessed using glibenclamide (KATP channels blocker). The study was approved by the Ethical Commitee of the Faculty of Medicine University J.J. Strossmayer Osijek. RESULTS: Results are shown as mean ± SEM (microns). For statistical analysis One way ANOVA was used. Control rats exhibit significant vasodilation in response to reduced pO2 (20± 4) compared to DM rats (0± 3) while vasodilation was restored in DM+HBOT rats (14± 2)). In the presence of clotrimazole, vasodilation to reduced pO2 was preserved in control group (18± 2), and attenuated in DM+HBOT (2± 1), similarly to impaired response in DM group (7± 3). Glibenclamide eliminated dilation in all groups. CONCLUSION: This study demonstrated that HBOT restored vasodilation in response to reduced pO2 in diabetic rats which is mediated via KATP channels, possibly due to effect of EETs on KATP channels. |
