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引言:全生命周期的睡眠呼吸障碍:利用动物模型探索一种人类疾病。

Introduction: Sleep-disordered breathing across the life span: exploring a human disorder using animal models.

作者信息

Gauda Estelle B

机构信息

Department of Pediatrics, Division of Neonatology, Johns Hopkins Medical Institutions, Baltimore, MD 21287-3200, USA.

出版信息

ILAR J. 2009;50(3):243-7. doi: 10.1093/ilar.50.3.243.

Abstract

Sleep-disordered breathing (SDB) is a constellation of breathing disorders that occur during sleep. Obstructive sleep apnea (OSA), the most common form, is characterized by complete or partial airway obstruction, hypoventilation, and central apneas, all of which lead to recurrent episodes of hypoxia, hypercapnia, sleep fragmentation, and elevated sympathetic tone. OSA occurs throughout the life span and is associated with significant cognitive, metabolic, and cardiovascular consequences that impair the quality of life. Building on observations that the upper airway collapses during sleep, obesity increases the risk of upper airway obstruction, and this obstruction leads to periods of hypoxia and reoxygenation that cause oxidative stress, researchers used large and small animal models to study the genetic predeterminants of OSA, the neuromechanical control of the upper airway during development and aging, and the metabolic consequences of oxidative stress. From the early canine models of experimentally induced upper airway obstruction to the current rodent models of intermittent hypoxia, the information now available has significantly improved scientists' understanding of the pathogenesis of OSA and its consequences, leading to better care for individuals with sleep-disordered breathing.

摘要

睡眠呼吸障碍(SDB)是指睡眠期间发生的一系列呼吸紊乱。阻塞性睡眠呼吸暂停(OSA)是最常见的形式,其特征为完全或部分气道阻塞、通气不足及中枢性呼吸暂停,所有这些都会导致反复出现缺氧、高碳酸血症、睡眠片段化以及交感神经张力升高。OSA在整个生命周期中均可发生,并伴有显著的认知、代谢和心血管后果,从而损害生活质量。基于睡眠期间上气道塌陷、肥胖会增加上气道阻塞风险以及这种阻塞会导致缺氧和再氧合期进而引起氧化应激的观察结果,研究人员使用大小动物模型来研究OSA的遗传决定因素、发育和衰老过程中上气道的神经机械控制以及氧化应激的代谢后果。从早期实验性诱导上气道阻塞的犬类模型到目前的间歇性缺氧啮齿动物模型,现有的信息显著提高了科学家对OSA发病机制及其后果的理解,从而为睡眠呼吸障碍患者提供更好的护理。

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