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Ventilatory chemoreflex sensitivity in sleep apnea is decreased with high dose ascorbic acid (1092.13)
Author(s) -
Leuenberger Urs,
Aswegen Caleb,
Blaha Cheryl,
Mast Jessica
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1092.13
Subject(s) - medicine , apnea , heart rate , blood pressure , ascorbic acid , microneurography , hypoxia (environmental) , intermittent hypoxia , endocrinology , anesthesia , obstructive sleep apnea , ventilation (architecture) , baroreflex , hypopnea , polysomnography , chemistry , oxygen , mechanical engineering , food science , organic chemistry , engineering
Obstructive sleep apnea (OSA) is associated with increased sympathetic activity, hypertension and augmented activity of the arterial chemoreflex. To test the hypothesis that oxidative stress, presumably due to intermittent hypoxia, contributes to these abnormalities, we determined blood pressure (BP), heart rate (HR), muscle sympathetic nerve activity (MSNA, peroneal microneurography), minute ventilation (MV) and the responses to 2‐8 breaths of nitrogen (N 2 , 10 trials aiming for O 2 saturation nadirs of 70‐90% [SpO 2 , oximetry]) before and after infusion of the antioxidant ascorbic acid (AA, 45 mg/kg over 20 min, followed by 15 mg/kg over 1 hr) in 8 patients with OSA (age 49±4 yrs, 7 male/1 female, apnea‐hypopnea‐index 42±10 events/hr). While AA did not affect BP (pre vs. post: 89±2 vs. 90±3 mmHg; P =NS), HR (pre vs. post: 67±5 vs. 66±4 beats/min; P =NS), MSNA (pre vs. post: 48±4 vs. 45±3 bursts/min; P =NS) and MV (pre vs. post: 11.1±0.8 vs. 11.6±0.9 L/min; P =NS), the ventilatory responses to N 2 induced transient hypoxia (expressed as the slope of peak MV vs. SpO 2 nadir) decreased from ‐0.372±0.059 pre‐AA to ‐0.288±0.058 L/min/%SpO 2 post‐AA ( P <0.05). Thus, ventilatory chemoreflex sensitivity which is thought to be enhanced in OSA decreases after AA. This suggests that the enhanced chemoreflex activity in patients with OSA is at least in part due to oxidative stress. Grant Funding Source : Supported by P01 HL096570 and UL1 TR000127