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  1. Article ; Online: Mechanisms of endothelial dysfunction in obstructive sleep apnea.

    Atkeson, Amy / Jelic, Sanja

    Vascular health and risk management

    2008  Volume 4, Issue 6, Page(s) 1327–1335

    Abstract: Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient ... ...

    Abstract Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic susceptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA.
    MeSH term(s) Animals ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Genetic Predisposition to Disease ; Humans ; Hypoxia/physiopathology ; Inflammation/complications ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Nitric Oxide/metabolism ; Oxidative Stress ; Oxygen/metabolism ; Risk Factors ; Sleep Apnea, Obstructive/complications ; Sleep Apnea, Obstructive/genetics ; Sleep Apnea, Obstructive/metabolism ; Sleep Apnea, Obstructive/physiopathology ; Sleep Deprivation/physiopathology
    Chemical Substances Inflammation Mediators ; Nitric Oxide (31C4KY9ESH) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2008-11-10
    Publishing country New Zealand
    Document type Journal Article ; Review
    ZDB-ID 2186568-1
    ISSN 1178-2048 ; 1176-6344
    ISSN (online) 1178-2048
    ISSN 1176-6344
    DOI 10.2147/vhrm.s4078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mechanisms of endothelial dysfunction in obstructive sleep apnea

    Amy Atkeson / Sanja Jelic

    Vascular Health and Risk Management, Vol 2008, Iss Issue 6, Pp 1327-

    2008  Volume 1335

    Abstract: Amy Atkeson, Sanja JelicDivision of Pulmonary, Allergy, and Critical Care Medicine, Columbia ...

    Abstract Amy Atkeson, Sanja JelicDivision of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NYAbstract: Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic suseptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA.Keywords: endothelial, obstructive sleep apnea, inflammation, dysfunction
    Keywords Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Cardiovascular ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2008-10-01T00:00:00Z
    Publisher Dove Medical Press
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Endothelial function in obstructive sleep apnea.

    Atkeson, Amy / Yeh, Susie Yim / Malhotra, Atul / Jelic, Sanja

    Progress in cardiovascular diseases

    2008  Volume 51, Issue 5, Page(s) 351–362

    Abstract: 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 ... ...

    Abstract 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.
    MeSH term(s) Animals ; Antioxidants/therapeutic use ; Blood Coagulation ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/physiopathology ; Cardiovascular Diseases/prevention & control ; Continuous Positive Airway Pressure ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Hemodynamics ; Humans ; Hypoxia/physiopathology ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Mandibular Advancement/instrumentation ; Nitric Oxide/metabolism ; Oxidative Stress ; Regeneration ; Sleep Apnea, Obstructive/complications ; Sleep Apnea, Obstructive/physiopathology ; Sleep Apnea, Obstructive/therapy ; Sleep Deprivation/physiopathology
    Chemical Substances Antioxidants ; Inflammation Mediators ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2008-12-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 209312-1
    ISSN 1873-1740 ; 1532-8643 ; 0033-0620
    ISSN (online) 1873-1740 ; 1532-8643
    ISSN 0033-0620
    DOI 10.1016/j.pcad.2008.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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