King's College London School of Medicine, London, UK.
Respir Physiol Neurobiol. 2010 Apr 15;171(1):54-60. doi: 10.1016/j.resp.2010.01.012. Epub 2010 Jan 29.
We wished to quantify, in patients with obstructive sleep apnoea (OSA), the activity of the respiratory muscles in relation to upper airway occlusion and patency in sleep. We hypothesized that particular levels of neuromuscular activation are directly associated with upper airway patency. 21 patients with previously diagnosed OSA and 21 healthy control subjects underwent respiratory muscle testing and polysomnography. Neural respiratory drive, as measured by the electromyogram of the diaphragm (EMG(di)) was elevated in the obese OSA patients, awake and supine (13.1(5.6)%max), compared to normal subjects (mean (SD) 8.1(2.3)%max, p<0.01). During unobstructed breathing in sleep (stage N2) normal subjects had an EMG(di) of 7.7(3.9) compared to 22.8(19.2)%max in the OSA group (p<0.001). Prior to airway occlusion, EMG(submandibular) and EMG(di) dropped markedly, and then, following occlusion, increased progressively to their highest levels at airflow onset. Patients with OSA require specific and increased levels of neural respiratory drive to sustain ventilation in sleep.
我们希望在患有阻塞性睡眠呼吸暂停（OSA）的患者中定量研究呼吸肌在睡眠时与上气道阻塞和通畅的关系。我们假设特定水平的神经肌肉激活与上气道通畅直接相关。21 名经诊断患有 OSA 的患者和 21 名健康对照者接受了呼吸肌测试和多导睡眠图检查。与正常对照组相比（平均值（标准差）为 8.1（2.3）%max，p<0.01），肥胖的 OSA 患者在清醒和仰卧位时膈肌肌电图（EMG(di)）的神经呼吸驱动升高（13.1（5.6）%max）。在睡眠期间（N2 期）无阻塞性呼吸时，正常对照组的 EMG(di)为 7.7（3.9），而 OSA 组为 22.8（19.2）%max（p<0.001）。在上气道阻塞之前，颏下肌 EMG 和 EMG(di)明显下降，然后在阻塞后，随着气流开始，逐渐增加到最高水平。OSA 患者需要特定的和增加的神经呼吸驱动水平来维持睡眠中的通气。
