文献类型：期刊文献

英文题名：Time-dependent sleep disruption at simulated 7000 m in rats: Delineating the compensation-to-decompensation transition

作者：Wang, Chang[1,2,3];Yan, Wen[1,3];Ma, Wenjuan[1,3];Zhang, Yinfei[1,3];Li, Xiping[1,3];Ma, Yuliang[3];Fang, Jingyang[3];Li, Wenbin[1,3];Wang, Rong[1,3]

第一作者：Wang, Chang

通信作者：Wang, R[1]

机构：[1]Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Peoples R China;[2]Lanzhou Univ, Hosp & Clin Med Sch 2, Dept Pharm, Lanzhou 730030, Peoples R China;[3]940th Hosp Joint Logist Support Force Chinese Peop, Dept Pharm, Lanzhou 730050, Peoples R China

第一机构：甘肃中医药大学药学院（西北中藏药协同创新中心办公室）

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Peoples R China.|[1073501e14fb35863569f]甘肃中医药大学药学院（西北中藏药协同创新中心办公室）;[10735]甘肃中医药大学;

年份：2026

卷号：315

外文期刊名：PHYSIOLOGY & BEHAVIOR

收录：;Scopus(收录号：2-s2.0-105045942209);WOS:【SSCI(收录号:WOS:001839279200001)，SCI-EXPANDED(收录号:WOS:001839279200001)】；

基金：Funding statement This study was supported by the Innovation Fund Project for College Teachers of Gansu Provincial Department of Education (2025B-024) , Gansu Provincial Major Project (23ZDFA013-5) , and the Natural Science Foundation of Gansu Province (23JRRA545) .

语种：英文

外文关键词：High-altitude sleep disorder; Hypobaric hypoxia; Sleep disruption; EEG; HPA axis; Rat model

摘要：High-altitude exposure disrupts sleep, but the temporal dynamics remain poorly defined. This study characterises time-dependent changes in sleep architecture, HPA axis function, inflammation, and central sleep-regulatory molecules during subacute hypobaric hypoxia. Male Sprague-Dawley rats were exposed to simulated 7000 m for 1, 3, 5, or 7 days (H1d-H7d). Sleep was recorded by wireless EEG/EMG. HPA axis hormones, inflammatory cytokines, and sleep-regulatory molecules were measured in serum, hippocampus, and hypothalamus. Multi-dimensional integration was performed using principal component analysis (PCA). Hypoxia progressively reduced total sleep time and sleep efficiency, increased REM sleep percentage, and fragmented wakefulness, accompanied by declines in SWS delta power and REM theta power. The HPA axis exhibited peripheral-central dissociation: serum ACTH increased, whereas hippocampal ACTH and CORT were suppressed. Peripheral inflammation followed a time-dependent pattern: an early IL-6 surge (H1d), sustained Th1 suppression (IL-12), and delayed IL-10 elevation (H7d). Hippocampal BDNF, GABA, and histamine progressively declined; hypothalamic PGD2, orexin A, 5-HT, and histamine similarly decreased, while dopamine increased at H5d-H7d. PCA indicated a temporal separation between H3d and H5d, suggesting a transition from compensation to decompensation (mean Q2 = 0.43). Subacute hypobaric hypoxia is associated with a time-dependent transition from compensation to decompensation, characterised by sleep architecture collapse, HPA axis uncoupling, phased inflammation, and progressive loss of central sleep-regulatory molecules. These findings offer a descriptive framework for understanding high-altitude sleep disorders.