Literature DB >> 22278815

Continuous positive airway pressure therapy improves vascular dysfunction and decreases oxidative stress in patients with the metabolic syndrome and obstructive sleep apnea syndrome.

Jun-ichi Oyama1, Hiroaki Yamamoto, Toyoki Maeda, Akira Ito, Koichi Node, Naoki Makino.   

Abstract

BACKGROUND: Patients with obstructive sleep apnea syndrome (OSAS) are always exposed to intermittent hypoxia and reoxygenation. The metabolic syndrome (MetS) and OSAS are also known to accelerate atherosclerosis, diabetes, and dyslipidemia. Therefore, nasal continuous positive airway pressure (CPAP) therapy may have beneficial effects in patients with the MetS and OSAS. HYPOTHESIS: This study in patients with the MetS and OSAS tested the validity of the hypothesis that chronic CPAP therapy improves factors involved in atherosclerosis, including impaired endothelial function.
METHODS: Thirty-two patients (19 males and 13 females, mean age 54 ± 9 y) diagnosed with the MetS and OSAS were enrolled in the study and received CPAP therapy for 3 months. Vascular function was investigated by measuring forearm blood flow (FBF) responses to reactive hyperemia (RH) using venous occlusion strain-gauge plethysmography. Biochemical markers were also measured before and after this procedure.
RESULTS: Basal apnea-hypopnea index was statistically correlated with FBF response to RH. The FBF response to RH was increased significantly after 3 months of CPAP therapy. A significant increase in plasma nitric oxide levels and a decrease in the levels of asymmetrical dimethylarginine, thiobarbituric acid reactive substance, soluble Fas ligand, and soluble CD40 ligand were detected after CPAP therapy. The plasma concentrations of tumor necrosis factor-α, interleukin (IL)-6, and IL-8 also decreased significantly with CPAP therapy, whereas IL-1β levels remained unchanged.
CONCLUSIONS: Continuous positive airway pressure therapy has beneficial effects on vascular function and inflammatory and oxidative stress in patients with the MetS and OSAS.
© 2012 Wiley Periodicals, Inc.

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Year:  2012        PMID: 22278815      PMCID: PMC6652717          DOI: 10.1002/clc.21010

Source DB:  PubMed          Journal:  Clin Cardiol        ISSN: 0160-9289            Impact factor:   2.882


  28 in total

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