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Sensorimotor nerve lesion of upper airway in patients with obstructive sleep apnea
Respiratory Physiology & Neurobiology ( IF 2.3 ) Pub Date : 2021-06-17 , DOI: 10.1016/j.resp.2021.103720
Xiangqiang Duan 1 , Meng Li 1 , Fei Liu 1 , Xianmin Song 1 , Caiyun Zhang 1 , Minhui Zhu 1 , Hongliang Zheng 1 , Shicai Chen 1
Affiliation  

The pathogenesis of obstructive sleep apnea (OSA) remains controversial. The role of anatomic stenosis is indisputable, and neural regulation of the upper airway remains to be elucidated. The upper airway maintains patency through the upper airway reflex. Lesions in any link of the reflex can increase the collapsibility of the upper airway. In this study, we investigated sensorimotor nerve lesions and their possible relationship with OSA. Tissue samples were obtained from the pharyngopalatine arch in 47 patients with OSA and 45 control participants to examine changes in the expression levels of myelin basic protein (MBP) and agrin through immunohistochemistry and western blotting. Downregulation of MBP in the mucosa reflects myelinated degeneration of mucosal sensory nerve axons, whereas upregulation of agrin in the neuromuscular junction reflects synaptic regeneration following denervation. The two neural factors correlate significantly with polysomnographic parameters, such as the apnea hypopnea index and lowest oxygen saturation. Our findings suggest that sensorimotor nerve damage in the upper airway of patients with OSA may be associated closely with the mechanism of OSA.



中文翻译:

阻塞性睡眠呼吸暂停患者上气道感觉运动神经病变

阻塞性睡眠呼吸暂停 (OSA) 的发病机制仍存在争议。解剖性狭窄的作用是无可争辩的,上气道的神经调节仍有待阐明。上呼吸道通过上呼吸道反射保持通畅。任何反射环节的病变都会增加上气道的塌陷性。在这项研究中,我们调查了感觉运动神经病变及其与 OSA 的可能关系。从 47 名 OSA 患者和 45 名对照参与者的咽腭弓获得组织样本,通过免疫组织化学和蛋白质印迹检查髓鞘碱性蛋白 (MBP) 和集聚蛋白表达水平的变化。粘膜中 MBP 的下调反映了粘膜感觉神经轴突的髓鞘变性,而神经肌肉接头中集聚蛋白的上调反映了去神经支配后的突触再生。这两个神经因素与多导睡眠图参数显着相关,例如呼吸暂停低通气指数和最低氧饱和度。我们的研究结果表明,OSA 患者上气道感觉运动神经损伤可能与 OSA 的发病机制密切相关。

更新日期:2021-06-19
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