Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea

Obstructive sleep apnoea (OSA) has been implicated as a risk factor for the development of hypertension, stroke and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflam...

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Bibliographic Details
Published in:Experimental physiology 2007-01, Vol.92 (1), p.51-65
Main Authors: Foster, Glen E., Poulin, Marc J., Hanly, Patrick J.
Format: Article
Language:English
Subjects:
Animals
Blood Vessels - physiopathology
Cardiovascular Diseases - etiology
Cerebrovascular Disorders - etiology
Disease Models, Animal
Humans
Hypoxia - complications
Hypoxia - physiopathology
Polysomnography
Risk Factors
Sleep Apnea, Obstructive - complications
Sleep Apnea, Obstructive - physiopathology
Time Factors
Vasoconstriction
Vasodilation
Vasomotor System - physiopathology
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Summary:Obstructive sleep apnoea (OSA) has been implicated as a risk factor for the development of hypertension, stroke and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflammation, atherosclerosis, endothelial dysfunction and hypertension. These proposed mechanisms have been drawn from basic research in animal and human models of intermittent hypoxia in addition to clinical investigation of patients with OSA. This review outlines the association between OSA and vascular disease, describes basic mechanisms that may be responsible for this association and compares the results from studies of OSA subjects with those in experimental models of intermittent hypoxia.
ISSN:0958-0670
1469-445X
DOI:10.1113/expphysiol.2006.035204