HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 103/2/608    most recent 01443.2006v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 (3) Citing Articles via Google Scholar Google Scholar Articles by Simmons, G. H. Articles by Halliwill, J. R. Search for Related Content PubMed PubMed Citation Articles by Simmons, G. H. Articles by Halliwill, J. R.

Systemic hypoxia causes cutaneous vasodilation in healthy humans

Department of Human Physiology, University of Oregon, Eugene, Oregon and HP2 Laboratory, INSERM ESPRI, Grenoble Medical School, France

Submitted 20 December 2006 ; accepted in final form 15 May 2007

Hypoxia and hypercapnia represent special challenges to homeostasis because of their effects on sympathetic outflow and vascular smooth muscle. In the cutaneous vasculature, even small changes in perfusion can shift considerable blood volume to the periphery and thereby impact both blood pressure regulation and thermoregulation. However, little is known about the influence of hypoxia and hypercapnia on this circulation. In the present study, 35 healthy subjects were instrumented with two microdialysis fibers in the ventral forearm. Each site was continuously perfused with saline (control) or bretylium tosylate (10 mM) to prevent sympathetically mediated vasoconstriction. Skin blood flow was assessed at each site (laser-Doppler flowmetry), and cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to baseline. In 13 subjects, isocapnic hypoxia (85 and 80% O₂ saturation) increased CVC to 120 ± 10 and 126 ± 7% baseline in the control site (both P < 0.05) and 113 ± 3 (P = 0.087) and 121 ± 4% baseline (P < 0.05) in the bretylium site. Adrenergic blockade did not affect the magnitude of this response (P > 0.05). In nine subjects, hyperpnea (matching hypoxic increases in tidal volume) caused no change in CVC in either site (both P > 0.05). In 13 subjects, hypercapnia (+5 and +9 Torr) increased CVC to 111 ± 4 and 111 ± 4% baseline, respectively, in the control site (both P < 0.05), whereas the bretylium site remained unchanged (both P > 0.05). Thus both hypoxia and hypercapnia cause modest vasodilation in nonacral skin. Adrenergic vasoconstriction of neural origin does not restrain hypoxic vasodilation, but may be important in hypercapnic vasodilation.

sympathetic nervous system; vascular resistance; microdialysis; skin; altitude; sleep apnea syndrome

This article has been cited by other articles:

				H. W. Kamendi, Q. Cheng, O. Dergacheva, J. G. Frank, C. Gorini, H. S. Jameson, R. A. Pinol, X. Wang, and D. Mendelowitz Recruitment of Excitatory Serotonergic Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus Post Hypoxia and Hypercapnia J Neurophysiol, March 1, 2008; 99(3): 1163 - 1168. [Abstract] [Full Text] [PDF]

				B. W. Wilkins, T. L. Pike, E. A. Martin, T. B. Curry, M. L. Ceridon, and M. J. Joyner Exercise intensity-dependent contribution of {beta}-adrenergic receptor-mediated vasodilatation in hypoxic humans J. Physiol., February 15, 2008; 586(4): 1195 - 1205. [Abstract] [Full Text] [PDF]

				G. H. Simmons, J. M. Manson, and J. R. Halliwill Mild central chemoreflex activation does not alter arterial baroreflex function in healthy humans J. Physiol., September 15, 2007; 583(3): 1155 - 1163. [Abstract] [Full Text] [PDF]