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OSAHS患者上气道及周围组织形态与功能改变的研究进展
阻塞性睡眠呼吸暂停(obstructive sleep apneahypopnea syndrome,OSAHS)是一种睡眠呼吸紊乱,表现为睡眠时反复的上气道塌陷.在气道塌陷时,发生通气降低(低通气,hypopnea)或停止(呼吸暂停,apnea),同时逐渐出现低氧血症和高碳酸血症.
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睡眠状态下阻塞性睡眠呼吸暂停低通气综合征患者上气道扩张肌肌电活性的变化
目的:观察睡眠状态下阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者上气道扩张肌肌电活性的变化,探讨其在OSAHS中的作用及意义.方法:对中、重度OSAHS患者69例(OSAHS组)及健康志愿者20例(对照组)于诱导睡眠后分别行颏舌肌、腭帆张肌和腭帆提肌等上气道扩张肌肌电图的检测并与诱导睡眠前比较.结果:①清醒状态下OSAHS组上气道扩张肌肌电水平较对照组高(均P<0.01);②与清醒状态比较,睡眠状态下OSAHS组上气道扩张肌肌电水平显著下降(均P<0.01);③从清醒状态到睡眠状态,OSAHS组上气道扩张肌肌电水平下降幅度明显大于对照组(均P<0.01).结论:OSAHS患者清醒状态下上气道扩张肌肌电活性代偿性升高及睡眠状态下失代偿是该病发生的重要病理生理机制.
关键词: 睡眠呼吸暂停低通气综合征 阻塞性 上气道扩张肌 肌电描记术 睡眠状态 -
OSAHS发病机制与治疗方式选择的探讨
OSAHS is a common disease during sleep and its pathogenesis is complex.The anatomic level of upper airway is a more recognized pathogenic factor.Recent studies have shown that nonanatomic factors,such as insufficiency in dilation muscles of upper airway,high loop gain and low arousal threshold,play an important role in the pathogenesis of OSAHS.This paper revives the latest literature home and abroad on the anatomical and nonanatomical factors in the pathogenesis of OSAHS and makes a systemic review.