Waltz Xavier, Beaudin Andrew E, Hanly Patrick J, Mitsis Georgios D, Poulin Marc J
Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
J Physiol. 2016 Dec 1;594(23):7089-7104. doi: 10.1113/JP272967.
Altered cerebral autoregulation (CA) in obstructive sleep apnoea (OSA) patients may contribute to increased stroke risk in this population; the gold standard treatment for OSA is continuous positive airway pressure, which improves cerebrovascular regulation and may decrease the risk of stroke. Isocapnic-hypoxia impairs CA in healthy subjects, but it remains unknown in OSA whether impaired CA is further exacerbated by isocapnic-hypoxia and whether it is improved by treatment with continuous positive airway pressure. During normoxia, CA was altered in the more severe but not in the less severe OSA patients, while, in contrast, during isocapnic-hypoxia, CA was similar between groups and tended to improve in patients with more severe OSA compared to normoxia. From a clinical perspective, one month of continuous positive airway pressure treatment does not improve CA. From a physiological perspective, this study suggests that sympathetic overactivity may be responsible for altered CA in the more severe OSA patients.
Cerebral autoregulation (CA) impairment may contribute to the increased risk of stroke associated with obstructive sleep apnoea (OSA). It is unknown if impaired CA is further exacerbated by isocapnic-hypoxia and whether it is improved by treatment of OSA with continuous positive airway pressure (CPAP). CA was assessed during wakefulness in 53 OSA patients (50.3 ± 9.3 years) and 21 controls (49.8 ± 8.6 years) at baseline and following a minimum of 1 month of effective CPAP therapy (OSA patients, n = 40). Control participants (n = 21) performed a follow-up visit to control for time effects within OSA patients between baseline and the post-CPAP visit. Beat-by-beat middle cerebral artery blood flow velocity and mean arterial blood pressure (MBP), and breath-by-breath end-tidal partial pressure of CO (P ET ,CO2) were monitored. CA was determined during normoxia and isocapnic-hypoxia using transfer function (phase and gain) and coherence analysis (including multiple and partial coherence (using MBP and P ET ,CO2 as inputs)) in the very low frequency range (0.03-0.07 Hz). OSA patients were divided into two subgroups (less severe and more severe) based upon the median respiratory disturbance index (RDI). During normoxia, the more severe OSA patients (RDI 45.9 ± 10.3) exhibited altered CA compared to controls and the less severe OSA patients (RDI 24.5 ± 5.9). In contrast, during isocapnic-hypoxia, CA was similar between groups. CPAP had no effect on CA. In conclusion, CA is altered in the more severe OSA patients during normoxia but not during isocapnic-hypoxia and CPAP treatment does not impact CA.
阻塞性睡眠呼吸暂停(OSA)患者的脑自动调节(CA)改变可能导致该人群中风风险增加;OSA的金标准治疗方法是持续气道正压通气,这可改善脑血管调节并可能降低中风风险。等碳酸血症性低氧会损害健康受试者的CA,但在OSA患者中,CA受损是否会因等碳酸血症性低氧而进一步加重,以及持续气道正压通气治疗是否能改善CA,目前尚不清楚。在常氧状态下,重度而非轻度OSA患者的CA发生改变,而相比之下,在等碳酸血症性低氧状态下,各组之间的CA相似,与常氧相比,重度OSA患者的CA有改善趋势。从临床角度来看,一个月的持续气道正压通气治疗并不能改善CA。从生理角度来看,本研究表明交感神经过度活跃可能是重度OSA患者CA改变的原因。
脑自动调节(CA)受损可能导致与阻塞性睡眠呼吸暂停(OSA)相关的中风风险增加。目前尚不清楚CA受损是否会因等碳酸血症性低氧而进一步加重,以及持续气道正压通气(CPAP)治疗OSA是否能改善CA。在基线时以及至少1个月的有效CPAP治疗后(OSA患者,n = 40),对53例OSA患者(50.3±9.3岁)和21例对照者(49.8±8.6岁)在清醒状态下进行CA评估。对照参与者(n = 21)进行随访,以控制OSA患者在基线和CPAP治疗后随访之间的时间效应。逐搏监测大脑中动脉血流速度和平均动脉血压(MBP),以及逐次呼吸的呼气末二氧化碳分压(PET,CO2)。在常氧和等碳酸血症性低氧状态下,使用传递函数(相位和增益)和相干分析(包括多重和偏相干(使用MBP和PET,CO2作为输入))在极低频范围(0.03 - 0.07Hz)测定CA。根据呼吸紊乱指数(RDI)中位数,将OSA患者分为两个亚组(轻度和重度)。在常氧状态下,与对照组和轻度OSA患者(RDI 24.5±5.9)相比,重度OSA患者(RDI 45.9±10.3)的CA发生改变。相比之下,在等碳酸血症性低氧状态下,各组之间的CA相似。CPAP对CA无影响。总之,在常氧状态下重度OSA患者的CA发生改变,但在等碳酸血症性低氧状态下未发生改变,且CPAP治疗不影响CA。