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Is there a delay in the activation of non‐noradrenergic vasoconstriction during cold exposure in human skin?

This study tested the hypothesis that cutaneous vasoconstriction during brief cold exposure occurs entirely through noradrenergic mechanisms. In 6 subjects, 2 microdialysis (MD) fibers were placed in the forearm skin. A control fiber received lactated ringers and the other received 5mM yohimbine (α‐adrenergic blockade). Skin blood flow was assessed at each site (laser‐Doppler flowmetry) and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure). Subjects were exposed to 10 min of cold stress (water‐perfused suit). CVC was reduced by 64 ± 9 % in the control site (P<0.05 vs. baseline) but unchanged in the yohimbine site during cold stress. In a follow‐up protocol (n=3) we added a third MD site with yohimbine + 1mM propranolol and extended the cold stress to 30 min. CVC was reduced in the control site throughout cold stress, but showed vasoconstriction during only the second half of the cold stress in both yohimbine and yohimbine + propranolol sites. Thus, short duration cold exposure can elicit cutaneous vasoconstriction mediated solely through noradrenergic mechanisms, whereas more prolonged cold stress also activates non‐noradrenergic vasoconstriction. Supported by the Evonuk and ACSM Foundations