Danish Center for Sleep Medicine, Department of Clinical Neurophysiology, Rigshospitalet, University of Copenhagen, Glostrup, Denmark.
Functional Imaging Unit, Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet, Glostrup, Denmark.
Sleep. 2018 Mar 1;41(3). doi: 10.1093/sleep/zsy001.
Obstructive sleep apnea (OSA) is associated with increased risk of stroke but the underlying mechanism is poorly understood. We suspect that the normal cerebrovascular response to hypoxia is disturbed in patients with OSA.
Global cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and lactate concentration during hypoxia were measured in patients with OSA and matched controls. Twenty-eight patients (82.1% males, mean age 52.3 ± 10.0 years) with moderate-to-severe OSA assessed by partial polysomnography were examined and compared with 19 controls (73.7% males, mean age 51.8 ± 10.1 years). Patients and controls underwent magnetic resonance imaging (MRI) during 35 min of normoxia followed by 35 min inhaling hypoxic air (10%-12% O2). After 3 months of continuous positive airway pressure (CPAP) treatment, 22 patients were rescanned.
During hypoxia, CBF significantly increased with decreasing arterial blood oxygen concentration (4.53 mL (blood)/100 g/min per -1 mmol(O2)/L, p < 0.001) in the control group, but was unchanged (0.89 mL (blood)/100 g/min per -1 mmol(O2)/L, p = 0.289) in the patient group before CPAP treatment. The CBF response to hypoxia was significantly weaker in patients than in controls (p = 0.003). After 3 months of CPAP treatment the CBF response normalized, showing a significant increase during hypoxia (5.15 mL (blood)/100 g/min per -1 mmol(O2)/L, p < 0.001). There was no difference in CMRO2 or cerebral lactate concentration between patients and controls, and no effect of CPAP treatment.
Patients with OSA exhibit reduced CBF in response to hypoxia. CPAP treatment normalized these patterns.
阻塞性睡眠呼吸暂停（OSA）与中风风险增加有关，但潜在机制尚不清楚。我们怀疑 OSA 患者的正常脑血管对缺氧的反应受到干扰。
通过部分多导睡眠图评估，对 28 例中重度 OSA 患者（82.1%男性，平均年龄 52.3±10.0 岁）和 19 例匹配对照者（73.7%男性，平均年龄 51.8±10.1 岁）进行了全球脑血流（CBF）、脑氧代谢率（CMRO2）和缺氧时乳酸浓度的测量。患者和对照者在 35 分钟的常氧期后进行磁共振成像（MRI）检查，然后在 35 分钟内吸入低氧空气（10%-12%O2）。在持续气道正压通气（CPAP）治疗 3 个月后，对 22 例患者进行了重新扫描。
在缺氧期间，随着动脉血氧浓度的降低，对照组的 CBF 显著增加（4.53 mL（血液）/100 g/min per -1 mmol(O2)/L，p<0.001），但在 CPAP 治疗前的患者组中无变化（0.89 mL（血液）/100 g/min per -1 mmol(O2)/L，p=0.289）。CPAP 治疗前患者的 CBF 对缺氧的反应明显弱于对照组（p=0.003）。CPAP 治疗 3 个月后，CBF 反应正常，在缺氧时显著增加（5.15 mL（血液）/100 g/min per -1 mmol(O2)/L，p<0.001）。患者和对照组之间的 CMRO2 或脑乳酸浓度无差异，CPAP 治疗也无影响。
OSA 患者在缺氧时 CBF 反应减少。CPAP 治疗使这些模式正常化。
