Inflammation, Oxidative Stress, and Repair Capacity of the Vascular Endothelium in Obstructive Sleep Apnea

• DOI: 10.1161/circulationaha.107.741512
• Publication Date: 2008-04-15T01:10:21Z
• Authors: Sanja Jelic; Margherita Padeletti; Steven M. Kawut; Christopher Higgins; Stephen M. Canfield; Duygu Onat; Paolo C. Colombo; Robert C. Basner; Phillip Factor; Thierry H. LeJemtel
• Keywords: Sleep

Background— Indirect evidence implicates endothelial dysfunction in the pathogenesis of vascular diseases associated with obstructive sleep apnea (OSA). We investigated directly whether and inflammation occur vivo endothelium patients OSA. The effects continuous positive airway pressure (CPAP) therapy on function repair capacity were assessed. Methods Results— Thirty-two newly diagnosed OSA 15 control subjects studied. Proteins that regulate basal nitric oxide (NO) production (endothelial NO synthase [eNOS] phosphorylated eNOS) (cyclooxygenase-2 inducible NOS) markers oxidative stress (nitrotyrosine) quantified by immunofluorescence freshly harvested venous cells before after 4 weeks CPAP therapy. Vascular reactivity was measured flow-mediated dilation. Circulating progenitor cell levels to assess capacity. Baseline expression eNOS reduced 59% 94%, respectively, compared subjects. Expression both nitrotyrosine cyclooxygenase-2 5-fold greater than subjects, whereas NOS 56% greater. significantly increased, nitrotyrosine, cyclooxygenase-2, decreased who adhered ≥4 hours daily. dilation lower increased Conclusions— affects promoting while decreasing availability Effective is reversal these alterations.