RT Journal Article
SR Electronic
T1 Fourteen nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP erj02042-2009
DO 10.1183/09031936.00204209
A1 R. Tamisier
A1 J.L. Pépin
A1 J. Rémy
A1 J.P. Baguet
A1 J.A. Taylor
A1 J.W. Weiss
A1 P. Lévy
YR 2010
UL http://erj.ersjournals.com/content/early/2010/06/04/09031936.00204209.abstract
AB Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterize the profile of this blood pressure increase, to determine if it is sustained, and to explore potential physiologic mechanisms.We performed 24 h ambulatory monitoring of blood pressure in 12 healthy subjects before and after two weeks of IH exposure. We also assessed systemic hemodynamics, muscle sympathetic nerve activity (MSNA), ischemic calf blood flow responses, and baroreflex gain. We obtained blood samples for inflammatory markers before, during, and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after two weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). MSNA increased across the exposure (17.2±5.1 vs. 21.7±7.3 burst·min−1 p<0.01) and baroreflex control of sympathetic outflow declined from −965.3±375.1 to −598.4±162.6 AIU.min−1.mmHg−1 (p<0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers.These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from lesser baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.