交感神经活性和血管内皮功能在阻塞性睡眠呼吸暂停低通气综合征合并高血压发病机制中的作用

Role of sympathetic nerve activity and arterial endothelial function in pathogenesis of hypertension in patients with obstructive sleep apnea-hypopnea syndrome

目的探讨交感神经活性、血管内皮功能在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并高血压发病机制中的作用。方法根据整夜多导睡眠监测(PSG)、血压测量和病史采集将93例患者分为:OSAHS 血压正常组、OSAHS 合并高血压组、高血压不合并 OSAHS 组和健康对照组。测定 PSG 当晚睡眠前后血压、血浆去甲肾上腺素、血浆内皮素和血清一氧化氮;收集 PSG 当晚22点至次晨6点的所有尿液送检尿3-甲氨基4-羟苦杏仁酸(VMA)。结果 OSAHS 组患者不论有无高血压,各指标变化为:晨起血浆去甲肾上腺素均显著高于睡前,OSAHS 合并高血压组升高更明显;醒后去甲肾上腺素与醒后平均动脉压、睡眠呼吸暂停低通气指数(AHI)、氧减次数、氧减指数、睡眠期间血氧饱和度低于90%的时间占总睡眠时间的百分比(T90)呈显著正相关,与睡眠时最低血氧饱和度(minSaO_2)和夜间平均血氧饱和度(MSaO_2)呈显著负相关;醒后内皮素显著增高、一氧化氮明显下降,而另外两组则相反;醒后内皮素与醒后平均动脉压、AHI、最长呼吸暂停时间、呼吸暂停总时间、氧减次数、氧减指数、T90呈显著正相关,与 minSaO_2、MSaO_2呈显著负相关;醒后一氧化氮与醒后平均动脉压、AHI、最长呼吸暂停时间、呼吸暂停总时间、氧减次数、氧减指数、T90呈显著负相关,与minSaO_2、MSaO_2呈显著正相关。各组间尿 VMA 无明显变化。结论在 OSAHS 患者夜间一过性血压升高和持续性高血压形成方面,交感神经系统活性增强、血管内皮功能紊乱导致的内皮源性舒、缩因子失衡可能起着重要的作用。

Objective To explore the role of sympathetic nerve activity and vessel endothelial function in the pathogenesis of hypertension in patients with obstructive sleep apnea-hypopnea syndrome （OSAHS）. Methods Based on polysomnography （PSG）, blood pressure （BP） and disease history, 93 subjects were divided into four groups： OSAHS with hypertension （OH）, OSAHS without hypertension （O）, hypertension without OSAHS （H）, normal control （N）. In addition to the blood pressure measurement, blood samples were collected before and after sleep during the PSG testing night to measure norepinephrine,endothelin, and NO levels. Urine samples were also collected during this time to test the level of vanillyl mandalic acid （VMA）. Results Patients in OH group and O group had significantly increased plasma NE value （P 〈0.05） in the next morning compared with those before sleep and the change was more significant in OH group compared to O group （ P〈0.01 ）. Pre-and after-sleep urine VMA levels in all groups showed no significant differences. Plasma NE and ET levels in OSAHS with and without hypertension after sleep were positively correlated with mean arterial pressure （MAP）, apnea-hypopnea index （ AH1）, number of oxygen desaturation ≥ 4% per hour （ ODI4 ）, percentage of time of oxygen saturation lower than 90% （T90） and correlated negatively with minimum arterial oxygen saturation （minSaO2） and mean arterial oxygen saturation （MSaO2 ）. Moreover, plasma ET also correlated positively with MAP, AHI, maximum apnea time, total apnea time. Compared with other groups plasma ET value increased significantly and serum NO value decreased in the next morning in both 0 and OH group. Serum NO value after one night sleep in both hypertensive and norhypertensive OSAHS patients was negatively correlated with MAP, AHI, maximum apnea time, total apnea time, ODI4, T90, and positively with minSaO2 and MSaO2. Conclusions Sympathetic nerve activation and endothelial dysfuntion characterized by an imbalance of endothelium-derived systolic and diastolic factors may play an important role in the development of transient and sustained increase of blood pressure in patients with OSAHS.