Endothelial Function in Obstructive Sleep Apnea

被引：121

作者：

Atkeson, Amy

Yeh, Susie Yim

Malhotra, Atul

Jelic, Sanja ^{[1
]}

机构：

[1] Columbia Univ Coll Phys & Surg, Div Pulm Allergy & Crit Care Med, Ctr PH8, New York, NY 10032 USA

来源：

PROGRESS IN CARDIOVASCULAR DISEASES | 2009年 / 51卷 / 05期

关键词：

POSITIVE AIRWAY PRESSURE; NITRIC-OXIDE SYNTHASE; ORAL APPLIANCE THERAPY; C-REACTIVE PROTEIN; NF-KAPPA-B; GROWTH-FACTOR; BLOOD-PRESSURE; PLASMA-LEVELS; PROGENITOR CELLS; INTERMITTENT HYPOXIA;

D O I：

10.1016/j.pcad.2008.08.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Untreated obstructive sleep apnea (OSA) is an independent risk factor for hypertension, myocardial infarction, and stroke. The repetitive hypoxia/reoxygenation and sleep fragmentation associated with OSA impair endothelial function. Endothelial dysfunction, in turn, may mediate increased risk for cardiovascular diseases. Specifically, in OSA, endothelial nitric oxide availability and repair capacity are reduced, whereas oxidative stress and inflammation are enhanced. Treatment of OSA improves endothelial vasomotor tone and reduces inflammation. We review the evidence and possible mechanisms of endothelial dysfunction as well as the effect of treatment on endothelial function in OSA. (C) 2009 Elsevier Inc. All rights reserved.

引用

收藏

页码：351 / 362

页数：12

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