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This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/H1668    most recent 00415.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Tartas, M. Articles by Abraham, P. Search for Related Content PubMed PubMed Citation Articles by Tartas, M. Articles by Abraham, P.

Early vasodilator response to anodal current application in human is not impaired by cyclooxygenase-2 blockade

¹Laboratory for Vascular Investigations and ²Laboratory of Biochemistry, University Hospital, and ³Centre National de la Recherche Scientifique UMR 6188, Physiology, University of Medicine, Angers Cedex, France

Submitted 10 May 2004 ; accepted in final form 18 November 2004

It is generally acknowledged that cutaneous vasodilatation in response to monopolar galvanic current application would result from an axon reflex in primary afferent fibers and the neurogenic inflammation resulting from neuropeptide release. Previous studies suggested participation of prostaglandin (PG) in anodal current-induced cutaneous vasodilatation. Thus the inducible cyclooxygenase (COX) isoform (COX-2), assumed to play a key role in inflammation, should be involved in the synthesis of the PG that is released. Skin blood flow (SkBF) variations induced by 5 min of 0.1-mA monopolar anodal current application were evaluated with laser-Doppler flowmetry on the forearm of healthy volunteers treated with indomethacin (COX-1 and COX-2 inhibitor), celecoxib (COX-2 inhibitor), or placebo. SkBF was indexed as cutaneous vascular conductance (CVC), expressed as percentage of heat-induced maximal CVC (%MVC). Urinalyses were performed to test celecoxib treatment efficiency. No difference was found in CVC values at rest: 14.3 ± 4.0, 11.9 ± 3.2, and 10.9 ± 2.0% MVC after indomethacin, celecoxib, and placebo treatment, respectively. At 10 min after the onset of anodal current application, CVC values were 22.2 ± 4.9% MVC (not significantly different from rest) with indomethacin, 85.7 ± 15.3% MVC (P < 0.001 vs. rest) with celecoxib, and 70.4 ± 13.1% MVC (P < 0.001 vs. rest) with placebo. Celecoxib significantly depressed the urinary prostacyclin metabolite 6-keto-PGF₁ (P < 0.05 vs. placebo). Indomethacin, but not celecoxib, significantly inhibited the anodal current-induced vasodilatation. Thus, although they are assumed to result from an axon reflex in primary afferent fibers and neurogenic inflammation, these results suggest that the early anodal current-induced vasodilatation is mainly dependent on COX-1-induced PG synthesis.

neurogenic inflammation; neuropeptide release; skin blood flow

This article has been cited by other articles:

				P. Rousseau, M. Tartas, B. Fromy, A. Godon, M.-A. Custaud, J. L. Saumet, and P. Abraham Platelet inhibition by low-dose aspirin but not by clopidogrel reduces the axon-reflex current-induced vasodilation in humans Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1420 - R1426. [Abstract] [Full Text] [PDF]