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阻塞性睡眠呼吸暂停患者内皮功能障碍的内皮机制。

Endothelial mechanisms of endothelial dysfunction in patients with obstructive sleep apnea.

机构信息

Respiratory Department of Tianjin Medical University General Hospital, Tianjin, 300052, China.

出版信息

Sleep Breath. 2012 Jun;16(2):283-94. doi: 10.1007/s11325-011-0519-8. Epub 2011 Apr 10.

DOI:10.1007/s11325-011-0519-8
PMID:21479903
Abstract

BACKGROUND

Obstructive sleep apnea (OSA) occurs in 2% of middle-aged women and 4% of middle-aged men in the general population and the prevalence is much higher in specific patient groups. Intermittent hypoxia (IH, oxygen desaturation and re-oxygenation) cycle, a major pathophysiologic character of OSA, and the physiological responses this evokes are thought to be responsible for its association with increased cardiovascular morbidity and mortality. Endothelial dysfunction, resulting from IH and as a key early event in atherosclerosis, was demonstrated repeatedly in patients with OSA and in animal models of IH, providing an important mechanistic link between the acute cyclical IH during sleep and the increased prevalence of chronic vascular diseases.

CONCLUSIONS

From this work, we conclude that IH from OSA may result in endothelial dysfunction, as a potential promoter of atherosclerosis, through nitric oxide unavailability, oxidative stress and inflammation, cell apoptosis, the crosstalk between endothelial cells and circulating inflammatory cells, microparticles, and damage repairing process. Though effective continuous positive airway pressure (CPAP) may specifically improve endothelial function, more controlled larger interventional trials that will include multiple centers and randomized allocation of CPAP therapy are needed to see if such changes are reversible before cause and effect can be implied finally, while further studies on cellular and animal level are also needed to elucidate molecular biologic/pathologic pathways.

摘要

背景

阻塞性睡眠呼吸暂停(OSA)在普通人群中,2%的中年女性和 4%的中年男性中发生,在特定患者群体中患病率更高。间歇性低氧(IH,氧饱和度下降和再氧合)循环是 OSA 的主要病理生理特征,其引起的生理反应被认为是其与心血管发病率和死亡率增加相关的原因。内皮功能障碍是由 IH 引起的,也是动脉粥样硬化的一个关键早期事件,在 OSA 患者和 IH 动物模型中反复得到证实,为睡眠期间急性周期性 IH 与慢性血管疾病患病率增加之间提供了重要的机制联系。

结论

从这项工作中,我们得出结论,OSA 的 IH 可能通过一氧化氮的不可用、氧化应激和炎症、细胞凋亡、内皮细胞和循环炎症细胞之间的串扰、微颗粒以及损伤修复过程导致内皮功能障碍,作为动脉粥样硬化的潜在促进因素。虽然有效的持续气道正压通气(CPAP)可能特异性地改善内皮功能,但需要更多的多中心、CPAP 治疗随机分组的对照性更大的干预试验,以观察这些变化是否在最终暗示因果关系之前是可逆的,同时还需要进一步在细胞和动物水平上的研究来阐明分子生物学/病理学途径。

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