Cerebral blood flow, oxygen metabolism, and lactate during hypoxia in patients with obstructive sleep apnea

• Published in: Sleep (New York, N.Y.) Vol. 41; no. 3
• Main Authors: Jensen, M L F, Vestergaard, M B, Tønnesen, P, Larsson, H B W, Jennum, Poul J
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.03.2018
• Subjects: Adult; Biomarkers - blood; Cerebrovascular Circulation - physiology; Continuous positive airway pressure; Continuous Positive Airway Pressure - methods; Female; Humans; Hypoxia; Hypoxia - blood; Hypoxia - diagnostic imaging; Hypoxia - physiopathology; Lactic Acid - blood; Male; Metabolism; Middle Aged; NMR; Nuclear magnetic resonance; Oxygen - blood; Polysomnography - methods; Sleep apnea; Sleep Apnea, Obstructive - blood; Sleep Apnea, Obstructive - diagnostic imaging; Sleep Apnea, Obstructive - physiopathology
• ISSN: 0161-8105; 1550-9109
• 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.