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, (P2α-VI, 22%, P
Original language | English |
---|---|
Pages (from-to) | 194-201 |
Number of pages | 8 |
Journal | Sleep |
Volume | 27 |
Issue number | 2 |
Publication status | Published - 2004 |
Externally published | Yes |
Keywords
- Apnea
- Hypoxia
- Oxidation
- Oxidative stress
- Wakefulness
ASJC Scopus subject areas
- Physiology