摘要目的:比较阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者阻塞型呼吸暂停（OSA）事件持续时间的整夜变化趋势，探讨机体对周期性呼吸紊乱的病理生理后果的适应能力及其潜在机制。方法:回顾性分析2018年10月至2019年12月于天津医科大学总医院睡眠中心进行多导睡眠监测（PSG）的打鼾患者89例，其中男61例，女28例，年龄23~74（44.5±12.7）岁，根据呼吸暂停低通气指数（AHI）将患者分为非OSAHS组（10例）、轻度OSAHS组（15例）、中度OSAHS组（29例）和重度OSAHS组（35例）。将整夜总记录时间平均分为4段，比较各组平均呼吸暂停持续时间（MAD）和最长呼吸暂停持续时间（LAD）随睡眠时段变化的趋势，并与人口学指标、脉搏血氧饱和度（SpO 2）指标和睡眠相关指标做相关性分析，此外绘制呼吸暂停次数-时间变化曲线进行拟合分析。 结果:重度OSAHS患者MAD为26.1（20.9，31.4）s，LAD为56.5（46.5，82.0）s，均显著高于非OSAHS、轻度OSAHS和中度OSAHS患者（ P<0.001），且重度OSAHS患者第3时段和第4时段MAD［分别为（28.4±9.0）和（27.3±9.8）s］显著高于第1时段［（22.3±9.9）s， P=0.046］，第3时段LAD［56.5（38.5，71.0）s］显著高于第1时段［41.0（28.0，53.0）s， P=0.018］。所有受试者第3时段和第4时段的MAD和LAD均显著高于第1时段［MAD分别为20.3（10.3，29.2）、18.5（11.3，24.2）和12.9（0.0，21.8）s， P<0.001；LAD分别为28.0（10.3，50.5）、28.0（12.0，44.5）和14.5（0.0，32.3）s， P<0.001］。所有受试者不同睡眠时段的最低SpO 2（LSpO 2）、平均SpO 2（MSpO 2）、SpO 2<90%的时间占总睡眠时间百分比（T90%）差异均无统计学意义（ P>0.05）。LAD与阻塞型呼吸暂停指数（OAI）呈正相关（ OR=1.660， P=0.025），其余各项指标与MAD、LAD均不相关（ P>0.05）。在睡眠起始（第1~31个OSA事件）平均每次呼吸暂停MAD增加0.22 s，此后平均每次呼吸暂停增加0.04 s，增加的速度减慢5.5倍。 结论:OSAHS患者MAD、LAD随睡眠时段的推移出现逐渐延长的趋势，且重度OSAHS患者延长趋势最明显，而SpO 2的动态变化趋势不明显。OSAHS患者可能存在多种对反复低氧发作的适应机制，且这种适应有阶段性，睡眠起始MAD快速增加，此后增加的速度明显减慢。重度OSAHS患者表现出最完全的变化形式，提示其病理生理改变最严重。

abstractsObjective:To compare the overnight variation trends in the duration of obstructive apnea events, and to explore the adaptive capacity to the pathophysiological consequences of periodic sleep disordered-breathing and its underlying mechanism in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods:A retrospective analysis were performed of the polysomnographic (PSG) results of 89 snoring patients including 10 non-OSAHS, 15 mild, 29 moderate and 35 severe OSAHS. The total record time was divided into four equal phases, and the variation trends of the mean apnea duration (MAD) and the longest apnea duration (LAD) were compared with the progression of sleep phases in different groups. Correlation analysis was conducted with demographic indicators, pulse oxygen saturation (SpO 2) and sleep related indicators. In addition, the number of apneas-time variability curve was plotted for fitting analysis. Results:In patients with severe OSAHS, both MAD [26.1(20.9, 31.4) s] and LAD [56.5(46.5, 82.0) s] were significantly higher than those of non-OSAHS, mild and moderate OSAHS ( P<0.001). In addition, the MAD in the third and fourth quartiles were significantly higher than that in the first quartile [(28.4±9.0) s, (27.3±9.8) s, (22.3±9.9) s, respectively, P=0.046], and the LAD in the third quartile was significantly higher than that in the first quartile [56.5(38.5, 71.0) s, 41.0(28.0, 53.0) s, respectively, P=0.018]. In all subjects, the MAD and LAD in the third and fourth quartiles were significantly higher than those in the first quartile [MAD: 20.3(10.3, 29.2) s, 18.5(11.3, 24.2) s, 12.9(0.0, 21.8) s, respectively, P<0.001; LAD: 28.0(10.3, 50.5) s, 28.0(12.0, 44.5) s, 14.5(0.0, 32.3) s, respectively, P<0.001]. There was no statistical difference in the lowest SpO 2 (LSpO 2), the mean SpO 2 (MSpO 2), and the percent of sleep time oxygen saturation below 90% (T90%) of all subjects in different sleep phases ( P>0.05). The LAD was positively correlated with obstructive apnea index (OAI, OR=1.660, P=0.025), but no correlation was observed with other indicators ( P>0.05). The MAD increased 0.22 s per episode at the onset of sleep (1-31 apnea events), then dropped to 0.04 s of increase per episode, with a dynamics change of 5.5-fold slower. Conclusions:The MAD and LAD show a gradual prolongation trend with the progression of sleep phases, and the prolongation trend is the most obvious in patients with severe OSAHS, while the dynamic change trend of SpO 2 is not obvious. There may be multiple adaptation mechanisms for recurrent hypoxic episodes, and the adaptation occurr in stages, with a rapid increase in MAD at the onset of sleep, follow by a markedly slower increase. Patients with severe OSAHS express the most complete pattern, suggesting the most severe pathophysiological outcomes.