期刊
PROGRESS IN CARDIOVASCULAR DISEASES
卷 51, 期 5, 页码 351-362出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.pcad.2008.08.002
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资金
- NHLBI NIH HHS [R01 HL085188, K24 HL093218, R01 HL073146] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K24HL093218, R01HL085188, R01HL073146] Funding Source: NIH RePORTER
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.
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