Long-term intermittent hypoxia in mice: Protracted hypersomnolence with oxidative injury to sleep-wake brain regions

Abstract

Study Objectives: This study was designed to test the hypothesis that long-term intermittent hypoxia (LTIH), modeling the hypoxia-reoxygenation events of sleep apnea, results in oxidative neural injury, including wake-promoting neural groups, and that this injury contributes to residual impaired maintenance of wakefulness. Design: Sleep times and oxidative-injury parameters were compared for mice exposed to LTIH and mice exposed to sham LTIH. Subjects: Adult male C57BL/6J mice were studied. Interventions: Mice were exposed to LTIH or sham LTIH in the lights-on period daily for 8 weeks. Electrophysiologic sleep-wake recordings and oxidative-injury measures were performed either immediately or 2 weeks following LTIH exposures. Measurements and Results: At both intervals, total sleep time per 24 hours in LTIH-exposed mice was increased by more than 2 hours, (P <05, and induction of antioxidant enzymes glutathione reductase and methionine sulfoxide reductase A, P