• Réka Füredi, Kata Bölcskei, János Szolcsányi, and Gábor Petho.
• Department of Pharmacology and Pharmacotherapy, University of Pécs, Szigeti út 12, H-7624 Pécs, Hungary.
• Life Sci. 2010 Feb 13; 86 (7-8): 244-50.

AimsPreviously we described the drop of the noxious heat threshold in response to mild heat injury or plantar incision. While mild heat injury elicits an immediate and short-lasting thermal hyperalgesia, surgical incision leads to a delayed and sustained heat hyperalgesia. Only very few peripheral mediators of these phenomena have been identified. Therefore the present study aimed at comparing the peripheral mediator background of heat hyperalgesia evoked by mild heat injury or surgical incision.Main MethodsHeat hyperalgesia was assessed by measuring the behavioural noxious heat threshold in conscious rats employing an increasing-temperature water bath.Key FindingsThe heat threshold drop evoked by a mild heat injury and measured 10min afterwards was reduced by intraplantarly applied HOE 140, a bradykinin B(2) receptor antagonist, NDGA, a non-selective lipoxygenase inhibitor, L-NOARG, a non-selective nitric oxide synthase inhibitor, TNP-ATP, a P2X purinoceptor antagonist and AMG9810, an antagonist of the transient receptor potential vanilloid type 1 (TRPV1) receptor. The heat threshold drop evoked by plantar incision and measured 18h later was reduced by intraplantarly applied HOE 140, [des-Arg(10)]-HOE 140, a bradykinin B(1) receptor antagonist, L-NOARG, TNP-ATP and the TRPV1 receptor antagonist SB-366791.SignificanceOnly small differences have been revealed between the examined peripheral mediators of the acute heat hyperalgesia evoked by mild heat injury and the sustained increase in heat responsiveness induced by surgical incision. The B(2) and B(1) bradykinin receptor, P2X purinoceptors, TRPV1 receptor, nitric oxide synthase and lipoxygenase(s) are involved in at least one of these hyperalgesia models.Copyright 2009 Elsevier Inc. All rights reserved.

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