Introduction: Endothelial dysfunction is an early risk factor for cardiovascular disease and hypertension. Mechanisms that participate in endothelial dysfunction include the decrease of nitric oxide (NO) and the increase of endothelin-1 (ET-1). ATP-sensitive potassium channels (KATP channels) also participate in endothelial cells in the vascular system. This study aims to investigate whether energy / ATP / SIRT1 is involved in endothelial dysfunction after the administration of hyperbaric oxygen (HBO).
Methods: This study was an experimental study, using a randomized post test only control group design using thirty white rats (Rattus norvegicus) Sprague dawley strains.There were 3 groups of p1, p2, and p3, and each group consists of 10 rats with the normal control for p1, high cholesterol diet for p2, and high cholesterol diet with hyperbaric oxygen of 2.4 ATA with 98% O2 for 3 sessions with the duration of 30 minutes / session, and air break for 5 minutes between each session for the period of 10 days consecutively for p3. The level of SIRT 1 was tested by using Elisa method. We applied statistical methods of investigation.
Results: The SIRT1 from ELISA results tend to increase after the administration of hyperbaric oxygen (HBO). Decreased of SIRT1 occur at group was given by high-cholesterol diet (p1=0,188Â±0,017 ng/ml; p2=0,114Â±0,029 ng/ml; p3=0,252Â±0,027 ng/ml). Hypercholesterolemia and endothelial dysfunction affect energy metabolism and reduce ATP levels and nicotinamide adenine dinucleotide (SIRT1). HBO therapy increases ATP and nicotinamide adenine dinucleotide levels which affect the increase of silent mating type information regulation two homologs 1, resulting in the optimal endothelial cell function.
Conclusion: Hyperbaric oxygen can significantly affect the endothelial dysfunction due to an high-cholesterol diet, by increasing the levels of Sirtuin-1.