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目的通过研究睡眠呼吸暂停综合征（ｏｂｓｔｒｕｃｔｉｖｅｓｌｅｐａｐｎｅａｓｙｎｄｒｏｍｅ，ＯＳＡＳ）腭咽软组织病理改变，探讨咽扩大肌在ＯＳＡＳ发病机理中的作用。方法对ＯＳＡＳ２７例，鼾症（ｓｉｍｐｌｅｓｎｏｒｉｎｇ，ＳＳ）１７例，对照（扁桃体摘除术患者）１５例的悬雍垂及腭咽肌进行ＨＥ、ＡＴＰ酶、还原型辅酶Ⅰ脱氢酶（ＮＡＤＨＴＲ）等染色，观察软组织病理结构改变。结果悬雍垂中部横截面所含肌肉百分比ＯＳＡＳ组明显低于ＳＳ组（Ｐ＜０．０５）；且与纤维组织百分比呈显著负相关；悬雍垂肌肌纤维总数量、Ⅰ型肌纤维数量、肌纤维面积及总面积，ＯＳＡＳ组均较ＳＳ组明显减少（Ｐ＜０．０５）；ＯＳＡＳ组腭咽肌Ⅰ型肌纤维所占百分比极其截面积明显低于对照组及ＳＳ组（Ｐ＜０．０５）。电镜下见ＯＳＡＳ肌原纤维结构紊乱，部分Ｚ带呈锯齿状排列，运动神经纤维水肿，轴突内出现空泡变性。结论ＯＳＡＳ患者咽扩大肌肌纤维萎缩、减少，肌肉自身功能紊乱可能是引起ＯＳＡＳ上气道异常塌陷的重要原因之一。
Objective To investigate the pathological changes of velopharyngeal soft tissues in obstructive sleep apnea syndrome (OSAS) and to explore the role of the pharyngeal enlarged muscles in the pathogenesis of OSAS. Methods HE, ATPase, reduced coenzyme Ⅰ dehydrogenase (NADHTR) were isolated from 27 cases of OSAS, 17 cases of simplesnoring (SS) and 15 cases of control (tonsillectomy) Dyeing, observation of soft tissue pathological changes. Results The percentage of muscular fibers in the middle uvula cross section was significantly lower than that in SS group (P <0.05), and negatively correlated with the percentage of fibrous tissue. The total number of uvula muscle myofibers, the number of type Ⅰ myofibers, (P <0.05). The percentage of type Ⅰ myofibers in OSAS group was significantly lower than that in control group and SS group (P <0.05) . Electron microscope, see OSAS myofibrillar structure disorders, some Z-band serrated arrangement, motor nerve fiber edema, vacuolar degeneration within axons. Conclusion OSAS patients with enlarged pharyngeal muscle fibers atrophy, decreased, muscle dysfunction may be caused by OSAS one of the important causes of abnormal collapse of the airways.