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1 Pulmonary and Sleep Research Laboratory, Division of Pulmonary, Critical Care & Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA; Laboratoire du Sommeil, Laboratoire HP2 (Hypoxie PathoPhysiologie), Centre Hospitalier Universitaire, Grenoble, France
2 Pulmonary and Sleep Research Laboratory, Division of Pulmonary, Critical Care & Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: rtamisie{at}bidmc.harvard.edu.
Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the post-exposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics (plethysmographic forearm blood flow (FBF), arterial pressure, heart rate) and peripheral chemosensitivity in normal volunteers on two occasions during and after two hours of either exposure. By design, mean SaO2 was lower during sustained relative to cyclic hypoxia. Baseline to recovery MSNA and mean arterial blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/mn p<0.01 and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg p<0.05 respectively after sustained hypoxia, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/mn and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg respectively after cyclic hypoxia. A significant increase in FBF occurred only after sustained but not cyclic hypoxia, from 2.3 ± 0.2 to 3.2 9 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml.min-1.100 gr of tissue-1 respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only MSNA but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.
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