Effect of whole-body and local heating on cutaneous vasoconstrictor responses in humans

Abstract

Animal studies suggest that α-adrenergic-mediated vasoconstriction is compromised during whole-body heating. The purpose of this study was to identify whether whole-body heating and/or local surface heating reduce cutaneous α-adrenergic vasoconstrictor responsiveness in human skin. Protocol I: Six subjects were exposed to neutral skin temperature (i.e., 34 °C), whole-body heating, and local heating of forearm skin to increase skin blood flow to the same relative magnitude as that observed during whole-body heating. Protocol II: In eight subjects forearm skin was locally heated to 34, 37, 40, and 42 °C. During both protocols, α-adrenergic vasoconstrictor responsiveness was assessed by local delivery of norepinephrine (NE) via intradermal microdialysis. Skin blood flow was continuously monitored over each microdialysis membrane via laser-Doppler flowmetry. In protocol I, whole-body and local heating caused similar increases in cutaneous vascular conductance (CVC). The EC 50 (log NE dose) of the dose–response curves for both whole body (−4.2±0.1 M) and local heating (−4.7±0.4 M) were significantly greater (i.e., high dose required to cause 50% reduction in CVC) relative to neutral skin temperature (−5.6±0.0 M; P<0.05 for both). In both local and whole-body heated conditions CVC did not return to pre-heating values even at the highest dose of NE. In protocol II, calculated EC 50 for 34, 37, 40, and 42 °C local heating was −5.5±0.4, −4.6±0.3, −4.5±0.3, −4.2±0.4 M, respectively. Statistical analyses revealed that the EC 50 for 37, 40 and 42 °C were significantly greater than the EC 50 for 34 °C. These results indicate that even during administration of high concentrations of NE, α-adrenergic vasoconstriction does not fully compensate for local heating and whole-body heating induced vasodilatation in young, healthy subjects. Moreover, these data suggest that elevated local temperatures, above 37 °C, and whole-body heating similarly attenuate cutaneous α-adrenergic vasoconstriction responsiveness.