alexa Obstructive Sleep Apnea Syndrome, Hypoxemia and Endothelial Dysfunction: One Disease or Many?
ISSN: 2161-105X

Journal of Pulmonary & Respiratory Medicine
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Review Article

Obstructive Sleep Apnea Syndrome, Hypoxemia and Endothelial Dysfunction: One Disease or Many?

Chitra Lal1*, Charlie Strange2

1Assistant Professor of Medicine, Medical University of South Carolina, Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, 96 Jonathan Lucas Street, CSB 812, MSC 630, Charleston, SC 29425, USA

2Professor of Medicine, Medical University of South Carolina, Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, 96 Jonathan Lucas Street, CSB 812, MSC 630, Charleston, SC 29425, USA

*Corresponding Author:
Chitra Lal, MD
Assistant Professor of Medicine
Medical University of South Carolina, Division of Pulmonary
Critical Care, Allergy and Sleep Medicine
96 Jonathan Lucas Street, CSB 812, MSC 630
Charleston, SC 29425, USA
Tel: 843 792 7776
E-mail: [email protected], [email protected]

Received date: September 08, 2011; Accepted date: October 17, 2011; Published date: October 19, 2011

Citation: Lal C, Strange C (2011) Obstructive Sleep Apnea Syndrome, Hypoxemia and Endothelial Dysfunction: One Disease or Many? J Pulmonar Respirat Med 1:101. doi: 10.4172/2161-105X.1000101

Copyright: © 2011 Lal C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

The significant adverse sequelae of Obstructive Sleep Apnea Syndrome (OSAS) include a higher incidence of stroke, myocardial infarction and neurocognitive deficits. A link between the intermittent hypoxia of OSAS and endothelial dysfunction may explain many of the macrovascular and microvascular complications of OSAS. The pathogenesis of endothelial dysfunction involves an alteration in the levels of pro-inflammatory and pro-atherogenic mediators. As a form of ischemia/reperfusion injury to the endothelium, intermittent hypoxia induces reactive oxygen species and dysregulatesbolites including pathways of nitric oxide synthesis. In addition, hypercoagulability and altered leucocyte migration contribute to the sp vasoactive metaectrum of endothelial dysfunction. The tools for measurement of endothelial dysfunction and its clinical implications are discussed. Endothelial dysfunction can be in part reversed with continuous positive airway pressure. Thus, early recognition and aggressive treatment of OSAS may prevent associated endothelial dysfunction and subsequent complications of this syndrome.

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