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, (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

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title = "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, (P2α-VI, 22%, P",

keywords = "Apnea, Hypoxia, Oxidation, Oxidative stress, Wakefulness",

author = "Veasey, {Sigrid Carlen} and Davis, {Christine W.} and Polina Fenik and Guanxia Zhan and Hsu, {Yeou Jey} and Domenico Pratico and Andrew Gow",

year = "2004",

language = "English",

volume = "27",

pages = "194--201",

journal = "Sleep",

issn = "0161-8105",

publisher = "American Academy of Sleep Medicine",

number = "2",

}

TY - JOUR

T1 - Long-term intermittent hypoxia in mice

T2 - Protracted hypersomnolence with oxidative injury to sleep-wake brain regions

AU - Veasey, Sigrid Carlen

AU - Davis, Christine W.

AU - Fenik, Polina

AU - Zhan, Guanxia

AU - Hsu, Yeou Jey

AU - Pratico, Domenico

AU - Gow, Andrew

PY - 2004

Y1 - 2004

N2 - 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

AB - 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

KW - Apnea

KW - Hypoxia

KW - Oxidation

KW - Oxidative stress

KW - Wakefulness

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