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1 Cardiovascular Diseases, Mayo Clinic and Mayo Foundation, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: somers.virend{at}mayo.edu.
Background: Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular disease, endothelial dysfunction, and increased 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. Methods and Results: 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 to 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=NS). Neither normal nor disturbed apneic sleep led to significant changes of plasma nitrotyrosine levels (morning levels: control group 0.14±0.01 ng/mL; OSA group 0.15±0.01 ng/mL, P=NS). Conclusions: 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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