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1 Department of Human Physiology, University of Oregon, Eugene, Oregon, United States
2 Faculté de Médecine de Grenoble, Laboratoire de Pharmacologie, HP2, France
* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.
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 current study, thirty-five 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 thirteen 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 effect 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 thirteen subjects, hypercapnia (+ 5 and + 9 torr) increased CVC to 111±4 and 111±4 % baseline in the control site (both P<0.05), while the bretylium site remained unchanged (both P>0.05). Thus, both hypoxia and hypercapnia cause modest vasodilation in non-acral skin. Adrenergic vasoconstriction of neural origin does not restrain hypoxic vasodilation, but may be important in hypercapnic vasodilation.
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