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一氧化氮(NO)水平在阻塞性睡眠呼吸暂停低通气综合征患者中的作用:一项荟萃分析。

The role of nitric oxide (NO) levels in patients with obstructive sleep apnea-hypopnea syndrome: a meta-analysis.

机构信息

Department of Otorhinolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

出版信息

Sleep Breath. 2021 Mar;25(1):9-16. doi: 10.1007/s11325-020-02095-0. Epub 2020 May 12.

DOI:10.1007/s11325-020-02095-0
PMID:32399702
Abstract

PURPOSE

The pathogenesis of cardiovascular disease (CVD) in patients with obstructive sleep apnea (OSA) is unclear. Several studies have suggested that CVD may be caused by oxidative stress from chronic intermittent hypoxia and associated vascular endothelial dysfunction. Oxidative stress in patients with OSA can induce endothelial cell apoptosis, aggravate vascular endothelial damage, and promote the expression of redox-sensitive genes and adhesion molecules. No meta-analysis has explored whether or not OSA is related to nitric oxide (NO).

METHOD

To assess the association between serum/plasma NO levels and OSA, we performed a meta-analysis of the literature on the subject to grade the strength of evidence.

RESULTS

OSA was significantly related to decreased serum or plasma NO levels (WMD = - 11.66, 95% CI - 17.21 to - 6.11; P < 0.01). Among the studies analyzed, there was high degree of heterogeneity (I = 79%, P < 0.01). Sensitivity analysis showed that after omitting any single study or converting a random effects model (REM) to a fixed effects model (FEM), the main results still held.

CONCLUSIONS

This meta-analysis suggests a strong correlation between OSA and serum or plasma NO levels which may explain the link between intermittent hypoxia of OSA and risk of CVD. The strength of this finding may spur further basic and clinical research into vascular endothelial dysfunction in patients with OSA.

摘要

目的

阻塞性睡眠呼吸暂停(OSA)患者心血管疾病(CVD)的发病机制尚不清楚。有几项研究表明,CVD 可能是由慢性间歇性低氧引起的氧化应激和相关的血管内皮功能障碍引起的。OSA 患者的氧化应激可诱导内皮细胞凋亡,加重血管内皮损伤,并促进氧化还原敏感基因和粘附分子的表达。目前尚无荟萃分析探讨 OSA 是否与一氧化氮(NO)有关。

方法

为了评估血清/血浆 NO 水平与 OSA 之间的关系,我们对该主题的文献进行了荟萃分析,以评估证据的强度。

结果

OSA 与血清或血浆 NO 水平降低显著相关(WMD = - 11.66,95%CI - 17.21 至 - 6.11;P < 0.01)。在分析的研究中,存在高度异质性(I = 79%,P < 0.01)。敏感性分析表明,在排除任何单项研究或将随机效应模型(REM)转换为固定效应模型(FEM)后,主要结果仍然成立。

结论

这项荟萃分析表明,OSA 与血清或血浆 NO 水平之间存在很强的相关性,这可能解释了 OSA 间歇性低氧与 CVD 风险之间的联系。这一发现的强度可能会激发进一步的基础和临床研究,以探讨 OSA 患者的血管内皮功能障碍。

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