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

TY - JOUR

T1 - Cerebral blood flow, oxygen metabolism, and lactate during hypoxia in patients with obstructive sleep apnea

AU - Jensen, M L F

AU - Vestergaard, M B

AU - Tønnesen, P

AU - Larsson, H B W

AU - Jennum, Poul J

PY - 2018/3/1

Y1 - 2018/3/1

N2 - Study Objectives 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. Methods Global cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO 2), 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% O 2). After 3 months of continuous positive airway pressure (CPAP) treatment, 22 patients were rescanned. Results During hypoxia, CBF significantly increased with decreasing arterial blood oxygen concentration (4.53 mL (blood)/100 g/min per -1 mmol(O 2)/L, p < 0.001) in the control group, but was unchanged (0.89 mL (blood)/100 g/min per -1 mmol(O 2)/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(O 2)/L, p < 0.001). There was no difference in CMRO 2 or cerebral lactate concentration between patients and controls, and no effect of CPAP treatment. Conclusions Patients with OSA exhibit reduced CBF in response to hypoxia. CPAP treatment normalized these patterns.

AB - Study Objectives 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. Methods Global cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO 2), 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% O 2). After 3 months of continuous positive airway pressure (CPAP) treatment, 22 patients were rescanned. Results During hypoxia, CBF significantly increased with decreasing arterial blood oxygen concentration (4.53 mL (blood)/100 g/min per -1 mmol(O 2)/L, p < 0.001) in the control group, but was unchanged (0.89 mL (blood)/100 g/min per -1 mmol(O 2)/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(O 2)/L, p < 0.001). There was no difference in CMRO 2 or cerebral lactate concentration between patients and controls, and no effect of CPAP treatment. Conclusions Patients with OSA exhibit reduced CBF in response to hypoxia. CPAP treatment normalized these patterns.

KW - Adult

KW - Biomarkers/blood

KW - Cerebrovascular Circulation/physiology

KW - Continuous Positive Airway Pressure/methods

KW - Female

KW - Humans

KW - Hypoxia/blood

KW - Lactic Acid/blood

KW - Male

KW - Middle Aged

KW - Oxygen/blood

KW - Polysomnography/methods

KW - Sleep Apnea, Obstructive/blood

U2 - 10.1093/sleep/zsy001

DO - 10.1093/sleep/zsy001

M3 - Journal article

C2 - 29309697

SN - 0161-8105

VL - 41

JO - Sleep

JF - Sleep

IS - 3

M1 - zsy001

ER -