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Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea
Author(s) -
Foster Glen E.,
Poulin Marc J.,
Hanly Patrick J.
Publication year - 2007
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2006.035204
Subject(s) - hypoxia (environmental) , intermittent hypoxia , medicine , cardiology , stroke (engine) , disease , myocardial infarction , oxidative stress , inflammation , obstructive sleep apnea , mechanical engineering , chemistry , organic chemistry , oxygen , engineering
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.