TY - JOUR
T1 - Effect of whole-body and local heating on cutaneous vasoconstrictor responses in humans
AU - Wilson, Thad E.
AU - Cui, Jian
AU - Crandall, Craig G.
N1 - Funding Information:
This research project was funded in part by grants from the National Aeronautics and Space Administration (NAG9-1033) and the National Heart, Lung, and Blood Institute (HL-61388 and HL-67422). Funding for TEW was provided via an Individual NSRA from the National Institutes of Health (HL-10488).
PY - 2002/5/31
Y1 - 2002/5/31
N2 - 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 EC50 (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 EC50 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 EC50 for 37, 40 and 42°C were significantly greater than the EC50 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.
AB - 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 EC50 (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 EC50 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 EC50 for 37, 40 and 42°C were significantly greater than the EC50 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.
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U2 - 10.1016/S1566-0702(02)00046-2
DO - 10.1016/S1566-0702(02)00046-2
M3 - Article
C2 - 12132645
AN - SCOPUS:0037204782
SN - 1566-0702
VL - 97
SP - 122
EP - 128
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
IS - 2
ER -