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Vol. 40, No. 4, 2003   

Free Abstract     Article (Fulltext)     Article (PDF 172 KB)     

Research Paper

Effect of Isoflurane on Skin-Pressure-Induced Vasodilation
Lionel Fizanne, Bérengère Fromy, Marie-Pierre Preckel, Dominique Sigaudo-Roussel, Jean Louis Saumet

Laboratory of Physiology, UPRES EA 2170, Department of Medicine, Angers, France

Address of Corresponding Author

J Vasc Res 2003;40:416-422 (DOI: 10.1159/000072890)


 goto top of page Key Words

  • Acetylcholine
  • Anesthesia
  • Endothelium
  • Iontophoresis
  • Laser Doppler
  • Mechanotransduction
  • Microcirculation
  • Rat
  • Skin blood flow
  • Sodium nitroprusside

 goto top of page Abstract

Since general anesthesia has been shown to attenuate endothelium-dependent vasodilation, it was of interest to verify whether general anesthesia would modify skin vasodilation in response to local pressure application, which is endothelium dependent. To study the effect of general anesthesia on pressure-induced vasodilation development, we examined the effects of low- and high-dose isoflurane. Skin blood flow was measured by laser Doppler flowmetry during 11.1 Pa s-1 increases in locally applied pressure in anesthetized rats treated with low or high doses of isoflurane. Following the administration of low doses of isoflurane, skin blood flow increased from baseline, with increasing local pressure application (+37 ± 10% at 2.0 kPa). The increase in skin blood flow was absent in rats treated with high doses (-20 ± 5% at 2.0 kPa), even when the anesthesia-induced hypotension was corrected by gelofusine infusion (-20 ± 10% at 2.0 kPa). Whereas sodium-nitroprusside-induced vasodilation developed following low and high doses of isoflurane, acetylcholine-induced vasodilation was impaired with high doses compared to low doses. These data show that pressure-induced vasodilation is abolished with high doses of anesthetics. It is not the anesthesia-induced hypotension, but the depth of anesthesia, which can lead to the disappearance of pressure-induced vasodilation by an alteration in endothelial function.

Copyright © 2003 S. Karger AG, Basel


 goto top of page Author Contacts

Prof. J.L. Saumet
Laboratory of Physiology
UPRES EA 2170, Department of Medicine
FR-49045 Angers Cedex (France)
Tel. +33 241 735845, Fax +33 241 735895, E-Mail jeanlouis.saumet@univ-angers.fr


 goto top of page Article Information

Received: May 23, 2003
Accepted after revision: June 6, 2003
Published online: August 12, 2003
Number of Print Pages : 7
Number of Figures : 3, Number of Tables : 3, Number of References : 28

 
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