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 |
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Keywords
- Apnea
- Hypoxia
- Oxidation
- Oxidative stress
- Wakefulness
ASJC Scopus subject areas
- Physiology
Cite this
Long-term intermittent hypoxia in mice : Protracted hypersomnolence with oxidative injury to sleep-wake brain regions. / Veasey, Sigrid Carlen; Davis, Christine W.; Fenik, Polina; Zhan, Guanxia; Hsu, Yeou Jey; Pratico, Domenico; Gow, Andrew.
In: Sleep, Vol. 27, No. 2, 2004, p. 194-201.Research output: Contribution to journal › Article
}
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
UR - http://www.scopus.com/inward/record.url?scp=3242744596&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3242744596&partnerID=8YFLogxK
M3 - Article
C2 - 15124711
AN - SCOPUS:3242744596
VL - 27
SP - 194
EP - 201
JO - Sleep
JF - Sleep
SN - 0161-8105
IS - 2
ER -