الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Obstructive sleep apnea (OSA) is characterized by repeated episodes of apnea during sleep. Each cycle of apnea and resumption of ventilation is accompanied by arterial oxyhaemoglobin desaturation and resaturation. This overnight repetitive hypoxia and reoxygenation may represent a form of oxidative stress, which generates reactive oxygen species. Many investigations, had established that OSA is an independent risk factor for many cardiovascular diseases. OSA is often associated with risk factors as aging, obesity, arterial hypertension, diabetes mellitus and ischemic heart disease. This increase in cardiovascular morbidity in patients with OSA is attributed to accelerated atherosclerosis. An early event of pathophysiologic importance in the atherosclerotic process is endothelial dysfunction.
Endothelial dysfunction is a broad term that was initially identified as impaired vasodilation due to diminished production or availability of nitric oxide (NO) and/or an imbalance in the relative contribution of endothelium-derived relaxing and contracting factors, such as endothelin-1 (ET-1), angiotensin, and oxidants. A broader understanding of the term would include not only reduced vasodilation but also a proinflammatory and prothrombic state associated with dysfunction of the endothelium.
Endothelial cells regulate leucocyte movement into tissues via carefully regulated processes involving adhesion molecules. Endothelial cells express E-selectin, P-selectin, ICAM-1 and VCAM-1. Adhesion molecules mediate the adhesion of leucocytes to the endothelium by binding to specific ligands on the leucocytes. VCAM-1 binds monocytes and T lymphocytes, the first step of invasion of the vessel wall by inflammatory cells. Once adherent, the monocytes transmigrate into the tunica intima, the innermost layer of the arterial wall. Once within the arterial intima, the monocytes develop into macrophages and begin to express scavenger receptors, that internalize modified lipoproteins. Internalization of these lipoprotein particles gives rise to lipid-laden macrophages or foam cells, which characterize early atherosclerotic lesions.
Oxidative stress may activate endothelial cells and leukocytes, resulting in increased expression of several glycoproteins, including the adhesion molecules as vascular cell adhesion molecule-1 (VCAM-1). This reactive oxygen species may also activate the oxidant-sensitive, proinflammatory transcription factor nuclear factor kappa β (NF-Kβ), increasing systemic inflammation. NF-κB is one of the most important redox responsive transcription factors, which has a role in the activation of the promoter activity of over 200 genes of many cytokines, growth factors, adhesion molecules and enzymes involved in immune and inflammatory responses, many of which play an important role in the pathophysiology of athrescleosis and other cardiovascular diseases.