Discipline of Physiology, School of Medical Sciences, University of Adelaide, Adelaide, 5000, South Australia, Australia; Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, 5041, South Australia, Australia.
Discipline of Physiology, School of Medical Sciences, University of Adelaide, Adelaide, 5000, South Australia, Australia; Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, 5041, South Australia, Australia; School of Medicine, Flinders University, Bedford Park, 5042, South Australia, Australia.
Sleep Med Rev. 2015 Aug;22:3-14. doi: 10.1016/j.smrv.2014.10.003. Epub 2014 Oct 15.
Intermittent hypoxia and unstable breathing are key features of obstructive sleep apnoea (OSA), the most common pathological problem of breathing in sleep. Unstable ventilatory control is characterised by high loop gain (LG), and likely contributes to cyclical airway obstruction by promoting airway collapse during periods of low ventilatory drive. Potential new strategies to treat OSA include manipulations designed to lower LG. However, the contribution of inherent versus induced LG abnormalities in OSA remains unclear. Hence, a better understanding of the mechanisms causing high LG in OSA is needed to guide the design of LG based treatments. OSA patients exhibit abnormal chemoreflex control which contributes to increased LG. These abnormalities have been shown to normalise after continuous positive airway pressure treatment, suggesting induced rather than inherent trait abnormalities. Experimental intermittent hypoxia, mimicking OSA, increases hypoxic chemosensitivity and induces long term facilitation; a sustained increase in ventilatory neural output which outlasts the original stimulus. These neuroplastic changes induce the same abnormalities in chemoreflex control as seen in OSA patients. This review outlines the evidence to support that a key component of high LG in OSA is induced by intermittent hypoxia, and is reversed by simply preventing this inducing stimulus.
间歇性低氧和呼吸不稳定是阻塞性睡眠呼吸暂停（OSA）的主要特征，这是睡眠中最常见的呼吸病理问题。不稳定的通气控制的特点是高环路增益（LG），并可能通过在通气驱动低的时期促进气道塌陷而导致周期性气道阻塞。治疗 OSA 的潜在新策略包括旨在降低 LG 的操作。然而，OSA 中固有 LG 与诱导性 LG 异常的贡献仍不清楚。因此，需要更好地了解导致 OSA 中 LG 升高的机制，以指导基于 LG 的治疗方法的设计。OSA 患者表现出异常的化学反射控制，这导致 LG 升高。已经表明，这些异常在持续气道正压通气治疗后恢复正常，这表明是诱导性而非固有特质异常。模拟 OSA 的实验性间歇性低氧会增加缺氧化学敏感性并诱导长期易化；通气神经输出的持续增加超过原始刺激。这些神经可塑性变化诱导与 OSA 患者所见相同的化学反射控制异常。这篇综述概述了支持 OSA 中高 LG 的一个关键组成部分是由间歇性低氧引起的，并通过简单地防止这种诱导性刺激而得到逆转的证据。
Zotero 插件