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Oxidative Stress Markers among Obstructive Sleep Apnea Patients

机译:阻塞性睡眠呼吸暂停患者的氧化应激标记

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Obstructive sleep apnea (OSA) is a chronic respiratory disorder, which can be present in up to 50% of the population, depending on the country. OSA is characterized by recurrent episodes of partial or complete obstruction of the upper airways with consistent movement of the respiratory musculature during sleep. Apneas and hypopneas can lead to a decrease in oxygen saturation, an increase in carbon dioxide in the blood, and subsequent arousals and sleep fragmentation caused by repetitive activation of the central nervous system. As a consequence, intermittent hypoxemia and consequent reoxygenation result in the production of reactive oxygen species, leading to systematic oxidative stress, which is postulated to be a key mechanism of endothelial dysfunction and increased risk for cardiovascular disorders in patients with OSA. In this review, various biomarkers of oxidative stress, including high-sensitivity C-reactive protein, pregnancy-associated plasma protein-A, superoxide dismutase, cell-free DNA, 8-hydroxy-2-deoxyguanosine, advanced oxidation protein products, lipid peroxidation products, receptor for advanced glycation end-products, and thioredoxin are discussed. Biomarkers of oxidative stress have the potential to be used to assess disease severity and treatment response. Continuous positive airway pressure (CPAP) is one of the most common noninvasive treatments for OSA; it keeps the upper airways open during sleep. This reduces episodes of intermittent hypoxia, reoxygenation, and arousal at night. CPAP has been shown to have anti-inflammatory properties and decrease oxidative stress. The administration of certain compounds, like vitamins A, C, and E as well as N-acetylcysteine and allopurinol, can decrease oxidative stress markers. However, their role in the treatment of OSA remains unclear.
机译:阻塞性睡眠呼吸暂停(OSA)是一种慢性呼吸系统障碍,可在最多50%的人口中,取决于国家。 OSA的特征在于,在睡眠期间,上呼吸道的部分或完全阻塞的局部或完全阻塞的剧集。呼吸暂停和低钠可导致氧饱和度降低,血液中二氧化碳的增加,以及随后的唤醒和睡眠碎片引起的中枢神经系统的重复激活引起的。因此,间歇性低氧血症和随后的雷氧化导致产生活性氧物质的产生,导致系统氧化应激,其假定为奥沙伊患者内皮功能障碍的关键机制和患者心血管障碍风险增加。在本文中,各种氧化应激的生物标志物,包括高灵敏度C反应蛋白,妊娠相关血浆蛋白-A,超氧化物歧化酶,无细胞DNA,8-羟基-2-脱氧核苷酸,晚期氧化蛋白质产品,脂质过氧化讨论了产品,高级糖化末端产物的受体,以及患有硫昔林。氧化胁迫的生物标志物具有用于评估疾病严重程度和治疗反应的可能性。连续正气道压力(CPAP)是OSA最常见的非侵入性治疗之一;它可以在睡眠期间保持上部通气道。这减少了夜间间歇性缺氧,重新氧化和唤醒的发作。 CPAP已被证明具有抗炎性能并降低氧化应激。施用某些化合物,如维生素A,C和E以及N-乙酰半胱氨酸和Allopurinol,可以降低氧化应激标记物。然而,它们在治疗OSA中的作用仍然不清楚。

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