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Vol. 43, No. 3, 2006   

Free Abstract     Article (Fulltext)     Article (PDF 244 KB)     

Free access is sponsored by an educational grant of the European Society for Microcirculation

Research Paper

Maximum Skin Hyperaemia Induced by Local Heating: Possible Mechanisms
Kim M. Goodinga, Michael M. Hannemanna, John E. Tookea, Geraldine F. Cloughb, Angela C. Shorea

aInstitute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, and
bDivision of Infection, Inflammation and Repair, School of Medicine, University of Southampton, Southampton, UK

Address of Corresponding Author

J Vasc Res 2006;43:270-277 (DOI: 10.1159/000091736)


 goto top of page Key Words

  • Maximum hyperaemia
  • Local heating
  • Nitric oxide
  • Prostaglandins
  • Histamine
  • Axon reflex

 goto top of page Abstract

Background: Maximum skin hyperaemia (MH) induced by heating skin to ge42°C is impaired in individuals at risk of diabetes and cardiovascular disease. Interpretation of these findings is hampered by the lack of clarity of the mechanisms involved in the attainment of MH. Methods: MH was achieved by local heating of skin to 42-43°C for 30 min, and assessed by laser Doppler fluximetry. Using double-blind, randomized, placebo-controlled crossover study designs, the roles of prostaglandins were investigated by inhibiting their production with aspirin and histamine, with the H1 receptor antagonist cetirizine. The nitric oxide (NO) pathway was blocked by the NO synthase inhibitor, NG-nitro-L-arginine methyl esther (L-NAME), and enhanced by sildenafil (prevents breakdown of cGMP). Results: MH was not altered by aspirin, cetirizine or sildenafil, but was reduced by L-NAME: median placebo 4.48 V (25th, 75th centiles: 3.71, 4.70) versus L-NAME 3.25 V (3.10, 3.80) (p = 0.008, Wilcoxon signed rank test). Inhibition of NO production (L-NAME) resulted in a more rapid reduction in hyperaemia after heating (p = 0.011), whereas hyperaemia was prolonged in the presence of sildenafil (p = 0.003). The increase in skin blood flow was largely confined to the directly heated area, suggesting that the role of heat-induced activation of the axon reflex was small. Conclusion: NO, but not prostaglandins, histamine or an axon reflex, contributes to the increase in blood flow on heating and NO is also a component of the resolution of MH after heating.

Copyright © 2006 S. Karger AG, Basel


 goto top of page Author Contacts

Dr. Kim Gooding
Diabetes and Vascular Medicine, Institute of Biomedical and Clinical Science
Peninsula Medical School, Barrack Road
Exeter EX2 5AX (UK)
Tel. +44 1392 403 081, Fax +44 1392 403 027, E-Mail kim.gooding@pms.ac.uk


 goto top of page Article Information

Received: August 4, 2005
Accepted after revision: December 17, 2005
Published online: February 22, 2006
Number of Print Pages : 8
Number of Figures : 5, Number of Tables : 0, Number of References : 38

 
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