Association of Cellular Adhesion Molecules and Oxidative Stress with Endothelial Function in Obstructive Sleep Apnea

Background: Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular disease (CVD). Several of the proposed mechanisms for the development of CVD in OSA are similar to those proposed for the increased risk of CVD in obesity, being difficult to determine the influence of OSA on these pathogenic mechanisms in obese individuals. Objectives: The purpose of this study was to evaluate the relationship of OSA with endothelial function, oxidative stress, inflammatory biomarkers, metabolic profile, sympathetic nervous system activity and blood pressure (BP) in obese individuals. Methods: In this cross-sectional study, were included 53 obese adults (28 women). Sleep study was performed with Watch-PAT200® and the diagnosis of OSA was made when apnea-hipopnea index (AHI) ≥5 events/h (n=33). All participants underwent evaluation of: body adiposity, BP, plasma catecholamines, high sensitivity C-reactive protein (hs-CRP), adiponectin, malondialdehyde, glucose, insulin, lipid profile and endothelial function (Endo-PAT 2000®). Results: Mean age (39.6 ± 1.5 vs. 32.5 ± 2.1y) and percentage of male participants (61% vs. 25%) were significantly higher in participants with OSA than in those without OSA (p=0.01). In univariate analysis participants with OSA compared with those without OSA exhibited higher values of neck circumference (40.98 ± 0.63 vs. 38.65 ± 0.75 cm, p=0.02), glucose (92.54 ± 1.97 vs. 80.2 ± 1.92 mg/dL, p=0.0001), noradrenaline (0.16±0.02 vs. 0.12±0.03 ng/mL, p=0.02) and systolic BP (126.05 ± 1.61 vs. 118.16 ± 1.86 mmHg, p=0.003). After adjustment for confounders, only glucose and hs-CRP were significantly higher in OSA patients. In correlation analysis, after controlling for confounders, AHI was associated with neck circumference (r=0.31,p=0.03) and hs-CRP (r=0.30,p=0.04), while minimum O2 saturation was associated with neck circumference (r=-0.31,p=0.03), insulin (r=-0.29,p=0.04) and HOMA-IR (r=-0.30,p=0.04). Conclusion: The present study suggests that in obese individuals OSA is associated with inflammation and worse glycemia; higher AHI correlates with increased central adiposity and inflammation; and lower oxygen saturation is related with insulin resistance.

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The Effect of Obstructive Sleep Apnea on DNA Damage and Oxidative Stress

Clinical and Experimental Otorhinolaryngology ◽

10.3342/ceo.2013.6.2.68 ◽

2013 ◽

Vol 6 (2) ◽

pp. 68 ◽

Cited By ~ 12

Author(s):

Il Gyu Kang ◽

Joo Hyun Jung ◽

Seon Tae Kim

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Obstructive Sleep ◽

And Oxidative Stress

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Nitric Oxide Bioavailability in Obstructive Sleep Apnea: Interplay of Asymmetric Dimethylarginine and Free Radicals

Sleep Disorders ◽

10.1155/2015/387801 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 4

Author(s):

Mohammad Badran ◽

Saeid Golbidi ◽

Najib Ayas ◽

Ismail Laher

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Endothelial Function ◽

Asymmetric Dimethylarginine ◽

Critical Role ◽

Middle Aged ◽

Obstructive Sleep

Obstructive sleep apnea (OSA) occurs in 2% of middle-aged women and 4% of middle-aged men and is considered an independent risk factor for cerebrovascular and cardiovascular diseases. Nitric oxide (NO) is an important endothelium derived vasodilating substance that plays a critical role in maintaining vascular homeostasis. Low levels of NO are associated with impaired endothelial function. Asymmetric dimethylarginine (ADMA), an analogue of L-arginine, is a naturally occurring product of metabolism found in the human circulation. Elevated levels of ADMA inhibit NO synthesis while oxidative stress decreases its bioavailability, so impairing endothelial function and promoting atherosclerosis. Several clinical trials report increased oxidative stress and ADMA levels in patients with OSA. This review discusses the role of oxidative stress and increased ADMA levels in cardiovascular disease resulting from OSA.

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The Effects of 1-Year Treatment With a Herbst Mandibular Advancement Splint on Obstructive Sleep Apnea, Oxidative Stress, and Endothelial Function

CHEST Journal ◽

10.1378/chest.06-0965 ◽

2007 ◽

Vol 131 (3) ◽

pp. 740-749 ◽

Cited By ~ 88

Author(s):

Sarah Itzhaki ◽

Hezi Dorchin ◽

Glenn Clark ◽

Lena Lavie ◽

Peretz Lavie ◽

...

Keyword(s):

Oxidative Stress ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Endothelial Function ◽

Mandibular Advancement ◽

Mandibular Advancement Splint ◽

Obstructive Sleep

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Circulating free nitrotyrosine in obstructive sleep apnea

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00241.2004 ◽

2004 ◽

Vol 287 (2) ◽

pp. R284-R287 ◽

Cited By ~ 38

Author(s):

Anna Svatikova ◽

Robert Wolk ◽

Hui H. Wang ◽

Maria E. Otto ◽

Kevin A. Bybee ◽

...

Keyword(s):

Oxidative Stress ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Nitrosative Stress ◽

Control Group ◽

Chromatography Tandem Mass Spectrometry ◽

Obstructive Sleep ◽

Before And After ◽

Liquid Chromatography Tandem Mass ◽

And Oxidative Stress

Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular disease, endothelial dysfunction, and oxidative stress, generated by repetitive nocturnal hypoxemia and reperfusion. Circulating free nitrotyrosine has been reported as a novel biomarker of nitric oxide (NO)-induced oxidative/nitrosative stress. Nitrosative stress has been implicated as a possible mechanism for development of cardiovascular diseases. We tested the hypothesis that repetitive severe hypoxemia resulting from OSA would increase NO-mediated oxidative stress. We studied 10 men with newly diagnosed moderate to severe OSA who were free of other diseases, had never been treated for OSA, and were taking no medications. Nitrotyrosine measurements, performed by liquid chromatography-tandem mass spectrometry, were made before and after untreated apneic sleep. We compared free nitrotyrosine levels in these patients with those obtained at similar times in 10 healthy male control subjects without OSA, with similar age and body mass index. Evening baseline nitrotyrosine levels were similar before sleep in the control and OSA groups [0.16 ± 0.01 and 0.15 ± 0.01 ng/ml, respectively, P = not significant (NS)]. Neither normal nor disturbed apneic sleep led to significant changes of plasma nitrotyrosine (morning levels: control group 0.14 ± 0.01 ng/ml; OSA group 0.15 ± 0.01 ng/ml, P = NS). OSA was not accompanied by increased circulating free nitrotyrosine either at baseline or after sleep. This observation suggests that repetitive hypoxemia during OSA does not result in increased NO-mediated oxidative/nitrosative stress in otherwise healthy subjects with OSA.

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