Meng Yanling, Li Wenyang, Zou Ying, Yao Ye, Huang Hong, Sun Jianjun, Li Xiaomeng, Guo Shu, Zhang Xilong, Wang Wei
Institute of Respiratory Disease, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Department of Plastic Surgery, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Nat Sci Sleep. 2020 Oct 15;12:749-758. doi: 10.2147/NSS.S249948. eCollection 2020.
Obstructive sleep apnea (OSA) is characterized by repetitive episodes of upper airway collapse during sleep. The contraction of upper airway dilator muscles plays a crucial role in maintaining UA patency. Chronic intermittent hypoxia (CIH) is the most important pathophysiological process of OSA. Exposure to CIH induced not only the damage of dilator muscles but also the plasticity of the muscles. This study aimed to dynamically assess the influence of CIH on the upper airway.
The experiments were performed on 44 rats. They were randomly divided into a normoxia (NO) group (n=22) and CIH group (n=22). In each group (n=6, respectively), EMG, transcranial magnetic stimulation (TMS) response, and critical pressure (Pcrit) value were recorded on day 0 (the day before exposure), and the 7th, 14th, 21st, and 28th day of air/CIH exposure. For each group, 16 rats were used for transmission electron microscopy observations on day 0, and the 7th, 14th and 28th day of air/CIH exposure (n=4 for every time point).
Compared to the NO group at the same point, the CIH group showed a damaged ultrastructure of genioglossus, increased activity of genioglossus corticomotor area, and increased Pcrit of the upper airway from the 7th to the 28th day of CIH. Increased EMG activity occurred at the 14th day of CIH and lasted for 2 weeks.
The elevated genioglossus corticomotor excitability in response to the CIH could not counterbalance the damage effect of CIH on upper airway dilator muscles, which ultimately increased the collapsibility of the upper airway.
阻塞性睡眠呼吸暂停（OSA）的特征是睡眠期间上呼吸道反复塌陷。上呼吸道扩张肌的收缩在维持上呼吸道通畅中起关键作用。慢性间歇性缺氧（CIH）是OSA最重要的病理生理过程。暴露于CIH不仅会导致扩张肌损伤，还会引起肌肉可塑性变化。本研究旨在动态评估CIH对上呼吸道的影响。
对44只大鼠进行实验。将它们随机分为常氧（NO）组（n = 22）和CIH组（n = 22）。每组分别于暴露前第0天、空气/CIH暴露第7天、第14天、第21天和第28天记录6只大鼠的肌电图（EMG）、经颅磁刺激（TMS）反应和临界压力（Pcrit）值。每组分别于暴露前第0天、空气/CIH暴露第7天、第14天和第28天取16只大鼠进行透射电子显微镜观察（每个时间点n = 4）。
与同一时间点的NO组相比，CIH组在CIH暴露第7天至第28天舌肌超微结构受损，舌肌皮质运动区活性增加，上呼吸道Pcrit升高。CIH暴露第14天出现EMG活性增加，并持续2周。
CIH引起的舌肌皮质运动兴奋性升高无法抵消CIH对上呼吸道扩张肌的损伤作用，最终增加了上呼吸道的塌陷性。
