Skin hyperemia induced by local heating : why is it blunted on repeat stimulations ?

Détails

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Etat: Public
Version: Après imprimatur
ID Serval
serval:BIB_39F0BB713D51
Type
Mémoire
Sous-type
(Mémoire de) maîtrise (master)
Collection
Publications
Institution
Titre
Skin hyperemia induced by local heating : why is it blunted on repeat stimulations ?
Auteur(s)
Herrmann C.
Directeur(s)
Feihl F.
Détails de l'institution
Université de Lausanne, Faculté de biologie et médecine
Statut éditorial
Acceptée
Date de publication
2011
Langue
anglais
Nombre de pages
16
Résumé
Background: In human skin, local heating produces local vasodilatation, a response termed thermal hyperemia. Thermal hyperemia is largely mediated by nitric oxide (NO). It is blunted on repeat stimulations applied to the same skin spot, a phenomenon termed desensitization. As this phenomenon could reflect a desensitization in the vasodilator effects of NO, we investigated whether a prior exposure to exogenous NO would result in an attenuated vasodilatory response to a subsequent thermal challenge. Methods: Thirteen healthy young men were studied. Skin blood flow (SkBF) was mesured on forearm skin with laser Doppler imaging. Exposure to exogenous NO was carried out by iontophoresis of sodium nitroprusside (SNP), a donor of NO. A local thermal stimulus (temperature step from 34 to 41°C maintained for 30 minutes) was applied with temperature-controlled chambers. We tested the influence of a previous transient exposure to exogenous NO on : 1) thermal hyperemia and 2) the response to a second identical exposure to exogeneous NO. Results: Thermal hyperemia (plateau SkBF at 30 minutes minus SkBF at 34°C) obtained on a site preexposed to exogenous NO two hours before was lower than obtained on a site preexposed to iontophoretic current only (mean±SD 395±139 perfusion units [PU] vs 540±79 PU ; p<0.01). When repeated on the same skin site two hours after the first one, exposure to exogenous NO led to a blunted vasodilatory response (298±121 PU vs 394±92 PU), although this difference was not statistically significant (p≈0.09). Conclusion: In forearm human skin, prior exposure to exogenous NO partially inhibits thermal hyperemia. These data support that desensitization of thermal hyperemia depends on a downregulation of the NO-cGMP pathway, possibly downstream from the endogenous production of NO.
Mots-clé
physiology, skin, blood flow, nitric oxide
Création de la notice
19/06/2012 11:41
Dernière modification de la notice
20/08/2019 14:29
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