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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/H2173    most recent 01021.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Gilmartin, G. Articles by Weiss, J. W. Search for Related Content PubMed PubMed Citation Articles by Gilmartin, G. Articles by Weiss, J. W.

Evidence of impaired hypoxic vasodilation after intermediate-duration hypoxic exposure in humans

¹Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts; and ²Sleep Laboratory, Grenoble University Hospital Hypoxia Pathophysiology Laboratory, Grenoble, France

Submitted 26 September 2005 ; accepted in final form 18 April 2006

Systemic hemodynamics, including forearm blood flow and ventilatory parameters, were evaluated in 21 subjects before and after exposure to 8 h of poikilocapnic hypoxia. To evaluate the role of sympathetic nervous system activation in the changes, in 10 of these subjects, we measured muscle sympathetic nerve activity (MSNA) before and after exposure, and the remaining 11 subjects received intra-arterial phentolamine infusion in the brachial artery to define vascular tone in the absence of sympathetically mediated vasoconstriction. Short-term ventilatory acclimatization occurred as evidenced by a decrease in resting PCO₂ (from 42 ± 1.4 to 37 ± 0.96 mmHg) and by an increase in the slope of the ventilatory response to acute hypoxia [from 0.7 ± 0.1 to 1.2 ± 0.2 l·min^–1·%Sp_O2 (blood O₂ saturation from pulse oximetry)] after exposure. Subjects demonstrated a significant increase in resting heart rate (from 61 ± 2 to 65 ± 2 beats/min) and diastolic blood pressure (from 64.8 ± 2.7 to 70.4 ± 2.0 mmHg). MSNA did not change significantly after exposure, although there was a trend toward a decrease in burst frequency (from 19.8 ± 4.1 to 14.3 ± 1.2 bursts/min). Forearm vascular resistance showed a significant decrease after termination of exposure (from 37.7 ± 3.6 to 27.6 ± 2.7 mmHg·ml^–1·min·100 g tissue, P < 0.05). Initially, progressive isocapnic hypoxia elicited significant vasodilation, but after 8 h of poikilocapnic hypoxic exposure, the acute challenge failed to change forearm vascular resistance. Local -blockade with phentolamine restored the vasodilatory response to acute hypoxia in the postexposure setting.

acclimatization; muscle sympathetic nerve activity; vascular resistance

This article has been cited by other articles:

				R. Tamisier, B. E. Hunt, G. S. Gilmartin, M. Curley, A. Anand, and J. W. Weiss Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3027 - H3035. [Abstract] [Full Text] [PDF]