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(Circulation. 1999;99:1183-1189.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Selective Potentiation of Peripheral Chemoreflex Sensitivity in Obstructive Sleep Apnea

Krzysztof Narkiewicz, MD, PhD; Philippe J. H. van de Borne, MD, PhD; Catherine A. Pesek, DO; Mark E. Dyken, MD; Nicola Montano, MD, PhD; Virend K. Somers, MD, PhD

From the Cardiovascular Division, Department of Internal Medicine (K.N., P.J.H.v.d.B., C.A.P., V.K.S.) and Department of Neurology (M.E.D.), University of Iowa College of Medicine, Iowa City, and Centro L.I.T.A. Vialba, Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedalè L. Sacco, Universitá degli Studi di Milano, Italy (N.M.).

Correspondence to Virend Somers, MD, PhD, Cardiovascular Division, Department of Internal Medicine, University of Iowa, 200 Hawkins Dr, Iowa City, IA 52242. E-mail virend-somers{at}uiowa.edu

Background—The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA.

Methods and Results—We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106±20%) was greater than in control subjects (52±23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24±6%) than in control subjects (7±5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects.

Conclusions—OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.


Key Words: nervous system • sleep • blood pressure • heart rate • hypoxia




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