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Cutaneous vasoconstriction during 30 minutes of progressive cold exposure is increased by hypoxia
Author(s) -
Simmons Grant H,
Minson Christopher T,
Halliwill John R
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.788.12
Subject(s) - vasoconstriction , hypoxia (environmental) , yohimbine , anesthesia , medicine , propranolol , cold stress , chemistry , oxygen , receptor , antagonist , biochemistry , organic chemistry , gene
The goal of this study was to test the effect of hypoxia on cutaneous vasoconstriction during prolonged cold exposure. Twelve subjects had 2 microdialysis fibers placed in the ventral forearm and were immersed to the sternum in a bathtub with arms positioned out of the water at heart level. One fiber was designated as control and the other received 5mM yohimbine + 1mM propranolol (to block adrenergic receptors). Skin blood flow was assessed at each site (laser‐Doppler flowmetry), divided by mean arterial pressure to calculate cutaneous vascular conductance (CVC), and scaled to baseline. Cold exposure was induced by a progressive reduction in water temperature from 36°C to 23°C over 30 minutes on 2 randomized study days (normoxia and poikilocapnic hypoxia [SaO 2 = 80%]). During normoxia, cold stress reduced CVC by 44 ± 4 and 13 ± 7 % baseline in control and yohimbine sites (both P < 0.05 vs. pre‐cooling). During hypoxia, cold stress reduced CVC by 67 ± 7 and 35 ± 11 % normoxic baseline in control and yohimbine sites (both P < 0.05 vs. pre‐cooling). Hypoxia increased the vasoconstrictor response at both sites (both P < 0.05 vs. normoxia). We conclude that hypoxia increases cutaneous vasoconstriction during prolonged cold exposure, and this effect is at least partially mediated through non‐noradrenergic mechanisms. Supported by the Evonuk and ACSM Foundations