Oxidative Stress Induces Endothelial Dysfunction and Endothelial Cell Damage in Rapid Eye Movement (REM) Sleep Deprivation Animal Model

Abstract

INTRODUCTION: Rapid eye movement (REM) sleep deprivation causes oxidative stress, leading to endothelial dysfunction, a predictor of cardiovascular disease. It is still unclear what causes endothelial dysfunction in patients with sleep disorder. This study evaluates the effects of REM sleep deprivation on the endothelium in the rat model of REM sleep deprivation. MATERIALS AND METHODS: Sprague-Dawley male rats (N=28) were divided into four groups (n=7); (1) free-moving control (FMC), (2) REM sleep deprivation (REMsd), (3) tank control (TC), and (4) sleep recovery (SR). The inverted flowerpot technique was utilised to develop REM sleep deprivation. Bodyweight gain (BWg), food consumption (Fc), and systolic blood pressure (SBP) were evaluated. The descending thoracic aorta was isolated to assess oxidative stress markers, in vitro functional study, and histomorphological examination. RESULTS: REM sleep deprivation showed a decrease in BWg significantly despite a significant increase in Fc, increased SBP, increased oxidative stress markers, caused endothelial dysfunction and endothelial cell damage. In REM sleep-deprived rats, there was a significant reduction in antioxidant markers, including total antioxidant capacity (TAC), superoxide dismutase (SOD) activity, catalase (CAT), and glutathione (GSH), while the levels of malondialdehyde (MDA) were significantly increased. The REM sleep-deprived rats displayed altered vascular function, including impaired vasorelaxation and hypercontractility. Histomorphology of the endothelium in REM sleep-deprived rats revealed features of endothelial damage. CONCLUSION: REM sleep deprivation is suggested to be linked to endothelial dysfunction due to endothelial damage. These changes are proposed to result from increased oxidative stress. Sleep recovery reduced the harmful effects following REM sleep deprivation.