Influence of hyperoxia on skin vasomotor control in normothermic and heat-stressed humans
- 1 December 2007
- journal article
- Published by American Physiological Society in Journal of Applied Physiology
- Vol. 103 (6), 2026-2033
- https://doi.org/10.1152/japplphysiol.00386.2007
Abstract
Hyperoxia induces skin vasoconstriction in humans, but the mechanism is still unclear. In the present study we examined whether the vasoconstrictor response to hyperoxia is through activated adrenergic function ( protocol 1) or through inhibitory effects on nitric oxide synthase (NOS) and/or cyclooxygenase (COX) ( protocol 2). We also tested whether any such vasoconstrictor effect is altered by body heating. In protocol 1 ( n = 11 male subjects), release of norepinephrine from adrenergic terminals in the forearm skin was blocked locally by iontophoresis of bretylium (BT). In protocol 2, the NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME) and the nonselective COX antagonist ketorolac (Keto) were separately administered by intradermal microdialysis in 11 male subjects. In the two protocols, subjects breathed 21% (room air) or 100% O2in both normothermia and hyperthermia. Skin blood flow (SkBF) was monitored by laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as the ratio of SkBF to blood pressure measured by Finapres. In protocol 1, breathing 100% O2decreased ( P < 0.05) CVC at the BT-treated and at untreated sites from the levels of CVC during 21% O2breathing both in normothermia and hyperthermia. In protocol 2, the administration of l-NAME inhibited ( P < 0.05) the reduction of CVC during 100% O2breathing in both thermal conditions. The administration of Keto inhibited ( P < 0.05) the reduction of CVC during 100% O2breathing in hyperthermia but not in normothermia. These results suggest that skin vasoconstriction with hyperoxia is partly due to the decreased activity of functional NOS in normothermia and hyperthermia. We found no significant role for adrenergic mechanisms in hyperoxic vasoconstriction. Decreased production of vasodilator prostaglandins may play a role in hyperoxia-induced cutaneous vasoconstriction in heat-stressed humans.Keywords
This publication has 42 references indexed in Scilit:
- Hyperoxia Attenuates Endothelial-Mediated Vasodilation in the Human SkinThe Journal of Physiological Sciences, 2007
- Spectral characteristics of skin sympathetic nerve activity in heat-stressed humansAmerican Journal of Physiology-Heart and Circulatory Physiology, 2006
- Relationship between ventilatory response and body temperature during prolonged submaximal exerciseJournal of Applied Physiology, 2006
- Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skinJournal of Applied Physiology, 2005
- Effects of regional phentolamine on hypoxic vasodilatation in healthy humansThe Journal of Physiology, 2001
- Influence of gender on the sympathetic neural adjustments to alterations in systemic oxygen levels in humansClinical Physiology and Functional Imaging, 1999
- Increases in Oxygen Tension Evoke Arteriolar Constriction by Inhibiting Endothelial Prostaglandin SynthesisMicrovascular Research, 1994
- Hypoxic Dilation of Coronary Arteries Is Mediated by ATP-Sensitive Potassium ChannelsScience, 1990
- The distribution of substance P-, CGRP-, galanin-and ANP-like immunoreactive nerves in human sweat glandsJournal of Molecular Histology, 1987
- EFFECTS OF OXYGEN BREATHING ON THE HEART RATE, BLOOD PRESSURE, AND CARDIAC INDEX OF NORMAL MEN—RESTING, WITH REACTIVE HYPEREMIA, AND AFTER ATROPINE*JCI Insight, 1962