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Impaired Vascular Regulation in Patients with Obstructive Sleep Apnea

Effects of Continuous Positive Airway Pressure Treatment

Kevin J. Reichmuth¹, John M. Dopp², Steven R. Barczi¹, James B. Skatrud^1,, Piotr Wojdyla¹, Don Hayes, Jr.¹ and Barbara J. Morgan³

¹ Departments of Medicine, School of Medicine and Public Health; ² Pharmacy Practice Division, School of Pharmacy, University of Wisconsin-Madison and Middleton Veterans Administration Hospital; and ³ Department of Orthopedics and Rehabilitation, School of Medicine and Public Health, University of Wisconsin-Madison and Middleton Veterans Administration Hospital, Madison, Wisconsin

Correspondence and requests for reprints should be addressed to Barbara J. Morgan, Ph.D., 1300 University Avenue, 5173 Medical Sciences Center, Madison, WI 53706-1532. E-mail: morgan{at}ortho.wisc.edu

Rationale: Impaired endothelium-dependent vasodilation has been documented in patients with sleep apnea. This impairment may result in blood flow dysregulation during apnea-induced fluctuations in arterial blood gases.

Objectives: To test the hypothesis that hypoxic and hypercapnic vasodilation in the forearm and cerebral circulation are impaired in patients with sleep apnea.

Methods: We exposed 20 patients with moderate to severe sleep apnea and 20 control subjects, to isocapnic hypoxia and hyperoxic hypercapnia. A subset of 14 patients was restudied after treatment with continuous positive airway pressure.

Measurements and Main Results: Cerebral flow velocity (transcranial Doppler), forearm blood flow (venous occlusion plethysmography), arterial pressure (automated sphygmomanometry), oxygen saturation (pulse oximetry), ventilation (pneumotachograph), and end-tidal oxygen and carbon dioxide tensions (expired gas analysis) were measured during three levels of hypoxia and two levels of hypercapnia. Cerebral vasodilator responses to hypoxia (–0.65 ± 0.44 vs. –1.02 ± 0.72 [mean ± SD] units/% saturation; P = 0.03) and hypercapnia (2.01 ± 0.88 vs. 2.57 ± 0.89 units/mm Hg; P = 0.03) were smaller in patients versus control subjects. Hypoxic vasodilation in the forearm was also attenuated (–0.05 ± 0.09 vs. –0.10 ± 0.09 unit/% saturation; P = 0.04). Hypercapnia did not elicit forearm vasodilation in either group. Twelve weeks of continuous positive airway pressure treatment enhanced hypoxic vasodilation in the cerebral circulation (–0.83 ± 0.32 vs. –0.46 ± 0.29 units/% saturation; P = 0.01) and forearm (–0.19 ± 0.15 vs. –0.02 ± 0.08 units/% saturation; P = 0.003), and hypercapnic vasodilation in the brain showed a trend toward improvement (2.24 ± 0.78 vs. 1.76 ± 0.64 units/mm Hg; P = 0.06).

Conclusions: Vasodilator responses to chemical stimuli in the cerebral circulation and the forearm are impaired in many patients with obstructive sleep apnea. Some of these impairments can be improved with continuous positive airway pressure.

Key Words: hypoxia • sleep • vasodilation • cerebral vascular circulation • regional blood flow

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Impaired hypoxic vasodilation in the cerebral circulation has been demonstrated in patients with obstructive sleep apnea (OSA). What This Study Adds to the Field Our study demonstrates that hypercapnic vasodilation in the cerebral circulation and hypoxic vasodilation in the forearm are impaired in patients with OSA. Furthermore, this study shows that such impairments are ameliorated by CPAP treatment.