期刊
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
卷 180, 期 10, 页码 1002-1009出版社
AMER THORACIC SOC
DOI: 10.1164/rccm.200905-0671OC
关键词
OSA; intermittent hypoxia; ventilation; oxidative stress
资金
- Alberta Heritage Foundation for Medical Research (AHFMR)
- Heart and Stroke Foundation of Alberta, NWT
- Canadian Foundation for Innovation
- Canadian Institutes of Health Research (CIHR)
- Focus-on-Stroke Program
- Hotchkiss Brain Institute
- TORCH (Tomorrow's Research Cardiovascular Health Professionals)
Rationale: Periodic occlusion of the upper airway in patients with obstructive sleep apnea leads to chronic intermittent hypoxia, which increases the acute hypoxic ventilatory response (AHVIR). Animal studies suggest that oxidative stress may modulate AHVR by increasing carotid body sensitivity to hypoxia. This has not been shown in humans. Objectives: To determine whether 4 days of exposure to chronic intermittent hypoxia increases AHVIR and oxidative stress and to determine the strength of the association between oxidative stress and AHVR. Methods: After two normoxic control days (Day -4 and Day 0), 10 young healthy men were exposed awake to 4 days (Days 1-4) of intermittent hypoxia for 6 hours per day. Measurements and Main Results: AHVR, assessed using an isocapnic hypoxia protocol, was determined as the slope of the linear regression between ventilation and oxygen desaturation. Oxidative stress was evaluated by measuring plasma DNA, lipid and protein oxidation, uric acid and antioxidant status by measuring a-tocopherol, total vitamin C, and antioxidant enzymatic activities. Between baseline and Day 4, there were significant increases in AHVR, DNA oxidation, uric acid, and vitamin C, whereas antioxidant enzymatic activities and alpha-tocopherol were unchanged. There were strong correlations between the changes in AHVR and DNA oxidation (r = 0.88; P = 0.002). Conclusions: Chronic intermittent hypoxia increases oxidative stress by increasing production of reactive oxygen species without a compensatory increase in antioxidant activity. This human study shows that reactive oxygen species overproduction modulates increased AHVR. These mechanisms may be responsible for increased AHVR in patients with obstructive sleep apnea.
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