Pathological Consequences of Intermittent Hypoxia in the Central Nervous System

被引:42
作者
Zhang, Shelley X. L. [1 ]
Wang, Yang [1 ]
Gozal, David [1 ]
机构
[1] Univ Chicago, Dept Pediat, Chicago, IL 60637 USA
基金
美国国家卫生研究院;
关键词
OBSTRUCTIVE SLEEP-APNEA; SPATIAL-LEARNING DEFICITS; APOE EPSILON-4 ALLELE; INDUCED OXIDATIVE STRESS; CHRONIC EPISODIC HYPOXIA; ISCHEMIC BRAIN-INJURY; NITRIC-OXIDE SYNTHASE; WORKING-MEMORY; ALZHEIMERS-DISEASE; NEUROCHEMICAL ALTERATIONS;
D O I
10.1002/cphy.c100060
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Intermittent hypoxia (IH) is a frequent occurrence in clinical settings. In the last decades, evidence has emerged implicating the gas exchange alterations and sleep disruption associated with those disorders in the high prevalence of cognitive and behavioral deficits afflicting these patients. In an effort to better characterize the role of IH, and to identify potential mechanisms of IH-induced central nervous system (CNS) dysfunction, a large number of rodent models have been recently developed. The cumulative evidence confirms that IH indeed induces a heterotopic pattern of injury in the brain, particularly affecting cortical, subcortical, and hippocampal regions, ultimately leading to neuronal apoptosis and activation of microglia. These IH-induced deleterious processes exhibit substantial variability across the lifespan, are under substantial modulatory influences of diet, physical or intellectual activity, and genetic factors, and preferentially recruit oxidative stress and inflammatory pathways. (C) 2012 American Physiological Society. Compr Physiol 2:1767-1777, 2012.
引用
收藏
页码:1767 / 1777
页数:11
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