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

Thad E. Wilson, Jian Cui, Craig G. Crandall

Research output: Contribution to journalArticle

66 Citations (Scopus)

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 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.

Original languageEnglish (US)
Pages (from-to)122-128
Number of pages7
JournalAutonomic Neuroscience: Basic and Clinical
Volume97
Issue number2
DOIs
StatePublished - May 31 2002

Fingerprint

Vasoconstrictor Agents
Heating
Skin
Adrenergic Agents
Norepinephrine
Vasoconstriction
Blood Vessels
Skin Temperature
Microdialysis
Forearm
Laser-Doppler Flowmetry
Vasodilation
Healthy Volunteers

Keywords

  • Alpha-adrenergic receptors
  • Cutaneous microdialysis
  • Heat stress
  • Norepinephrine

ASJC Scopus subject areas

  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems

Cite this

Effect of whole-body and local heating on cutaneous vasoconstrictor responses in humans. / Wilson, Thad E.; Cui, Jian; Crandall, Craig G.

In: Autonomic Neuroscience: Basic and Clinical, Vol. 97, No. 2, 31.05.2002, p. 122-128.

Research output: Contribution to journalArticle

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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 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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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.

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