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Am. J. Respir. Crit. Care Med., Volume 161, Number 1, January 2000, 187-191

Vascular Reactivity in Obstructive Sleep Apnea Syndrome

HANS W. DUCHNA, CHRISTIAN GUILLEMINAULT, RICCARDO A. STOOHS, JOHN L. FAUL, HEITOR MORENO, BRIAN B. HOFFMAN, and TERENCE F. BLASCHKE

Stanford Sleep Disorders Center and Division of Clinical Pharmacology, Stanford University Medical Center, Stanford, California; and Geriatric Research, Education and Clinical Center, VA Medical Center, Palo Alto, California

The obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular disease and systemic hypertension. Because systemic arterial blood pressure is proportional to venodilation and venous return to the heart, we hypothesized that altered vascular responsiveness might exist in the veins of subjects with OSAS. We therefore investigated venodilator responses in awake, normotensive subjects with and without OSAS, using the dorsal hand vein compliance technique. Dose-response curves to bradykinin and nitroglycerin were obtained from 12 subjects with OSAS and 12 matched control subjects. Maximal dilation (Emax) to bradykinin was significantly lower in the OSAS group (62.1% ± 26.1%) than in the control group (94.3% ± 10.7%) (p < 0.005). Vasodilation to nitroglycerin tended to be lower in the OSAS group (78.6% ± 31.8%) than the control group (100.3% ± 12.9%), but this effect did not reach statistical significance. When six of the OSAS subjects were retested after 60 d of treatment with nasal continuous positive airway pressure (CPAP), Emax to bradykinin rose from 60.3% ± 20.3% to 121.4% ± 26.9% (p < 0.01). Vasodilation to nitroglycerin also increased, but this effect did not reach statistical significance. These results demonstrate that a blunted venodilatory responsiveness to bradykinin exists in OSAS. This effect appears to be reversible with nasal CPAP therapy. Duchna HW, Guilleminault C, Stoohs RA, Faul JL, Moreno H, Hoffman BB, Blaschke TF. Vascular reactivity in obstructive sleep apnea syndrome.




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