Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea

Exp Physiol. 2007 Jan;92(1):51-65. doi: 10.1113/expphysiol.2006.035204. Epub 2006 Nov 23.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • 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*