间歇性缺氧诱导的炎症与阻塞性睡眠呼吸暂停低通气综合征中呼出挥发性有机化合物谱的形成：一篇叙述性综述

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中文摘要

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）以睡眠期间反复上气道阻塞、间歇性缺氧（IH）和睡眠碎片化为特征，并与氧化应激、慢性低度炎症、代谢紊乱和上气道重塑相关。这些病理生理紊乱可能改变挥发性代谢物的生成和释放，从而为研究呼出挥发性有机化合物（VOC）谱作为OSAHS相关氧化还原失衡、炎症活动和代谢异常的无创指标提供了依据。本综述以IH诱导的炎症反应为核心机制环节，探讨炎症导致OSAHS呼出VOC谱变化的潜在机制。反复缺氧-复氧和上气道机械应力可能激活炎症信号通路，包括核因子κB、缺氧诱导因子-1α和NOD样受体家族含pyrin结构域3，并可能通过放大的氧化应激、脂质过氧化、代谢重编程和局部气道微环境改变，影响醛类、烷烃、丙酮、醇类和异戊二烯等挥发性代谢物的生成和释放。现有临床研究表明，OSAHS患者的呼出VOC谱可能与疾病严重程度、夜间缺氧负荷、代谢异常和治疗反应相关。然而，候选VOC的特异性和可重复性仍受个体代谢谱、外源性暴露和方法学异质性的限制。未来研究应整合标准化呼气采样、高置信度化合物鉴定、纵向验证以及炎症、氧化应激和代谢标志物的同步评估。炎症相关VOC谱分析可能为OSAHS的病理生理异质性提供机制见解，并支持无创评估工具和更个性化管理策略的开发。

英文摘要

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by recurrent upper airway obstruction during sleep, intermittent hypoxia (IH), and sleep fragmentation, and is associated with oxidative stress, chronic low-grade inflammation, metabolic dysregulation, and upper airway remodeling. These pathophysiological disturbances may alter the generation and release of volatile metabolites, thereby providing a rationale for investigating exhaled volatile organic compound (VOC) profiles as noninvasive indicators of OSAHS-related redox imbalance, inflammatory activity, and metabolic abnormalities. Focusing on IH-induced inflammatory responses as a central mechanistic link, this review examines the potential mechanisms through which inflammation contributes to changes in exhaled VOC profiles in OSAHS. Repeated hypoxia-reoxygenation and upper airway mechanical stress may activate inflammatory signaling pathways, including nuclear factor κB, hypoxia-inducible factor-1α, and NOD-like receptor family pyrin domain-containing 3, and may influence the generation and release of volatile metabolites such as aldehydes, alkanes, acetone, alcohols, and isoprene through amplified oxidative stress, lipid peroxidation, metabolic reprogramming, and alterations in the local airway microenvironment. Available clinical studies suggest that exhaled VOC profiles in patients with OSAHS may be associated with disease severity, nocturnal hypoxic burden, metabolic abnormalities, and treatment response. However, the specificity and reproducibility of candidate VOCs remain limited by individual metabolic profiles, exogenous exposures, and methodological heterogeneity. Future studies should integrate standardized breath sampling, high-confidence compound identification, longitudinal validation, and concurrent assessment of inflammatory, oxidative stress, and metabolic markers. Inflammation-related VOC profiling may offer mechanistic insight into the pathophysiological heterogeneity of OSAHS and support the development of noninvasive assessment tools and more personalized management strategies.