Comparison of the peripheral mediator background of heat injury- and plantar incision-induced drop of the noxious heat threshold in the rat

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Abstract

Aims: Previously 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 methods: Heat hyperalgesia was assessed by measuring the behavioural noxious heat threshold in conscious rats employing an increasing-temperature water bath. Key findings: The heat threshold drop evoked by a mild heat injury and measured 10min afterwards was reduced by intraplantarly applied HOE 140, a bradykinin B2 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-Arg10]-HOE 140, a bradykinin B1 receptor antagonist, L-NOARG, TNP-ATP and the TRPV1 receptor antagonist SB-366791. Significance: Only 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 B2 and B1 bradykinin receptor, P2X purinoceptors, TRPV1 receptor, nitric oxide synthase and lipoxygenase(s) are involved in at least one of these hyperalgesia models.

Original languageEnglish
Pages (from-to)244-250
Number of pages7
JournalLife Sciences
Volume86
Issue number7-8
DOIs
Publication statusPublished - febr. 2010

Fingerprint

Rats
Hot Temperature
Wounds and Injuries
Hyperalgesia
Nitroarginine
Nitric Oxide Synthase
Purinergic P2X Receptor Antagonists
Purinergic P2X Receptors
Bradykinin B1 Receptors
Bradykinin B2 Receptors
Purinergic P2 Receptors
Lipoxygenase Inhibitors
Lipoxygenase
Baths

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{d27333a489c64510b16ae30a6a6ec0dd,
title = "Comparison of the peripheral mediator background of heat injury- and plantar incision-induced drop of the noxious heat threshold in the rat",
abstract = "Aims: Previously 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 methods: Heat hyperalgesia was assessed by measuring the behavioural noxious heat threshold in conscious rats employing an increasing-temperature water bath. Key findings: The heat threshold drop evoked by a mild heat injury and measured 10min afterwards was reduced by intraplantarly applied HOE 140, a bradykinin B2 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-Arg10]-HOE 140, a bradykinin B1 receptor antagonist, L-NOARG, TNP-ATP and the TRPV1 receptor antagonist SB-366791. Significance: Only 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 B2 and B1 bradykinin receptor, P2X purinoceptors, TRPV1 receptor, nitric oxide synthase and lipoxygenase(s) are involved in at least one of these hyperalgesia models.",
keywords = "Heat hyperalgesia, Heat injury, Inflammatory mediators, Noxious heat threshold, Plantar incision, TRPV1 receptor",
author = "R{\'e}ka F{\"u}redi and K. B{\"o}lcskei and J. Szolcs{\'a}nyi and G. Pethő",
year = "2010",
month = "2",
doi = "10.1016/j.lfs.2009.12.010",
language = "English",
volume = "86",
pages = "244--250",
journal = "Life Sciences",
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TY - JOUR

T1 - Comparison of the peripheral mediator background of heat injury- and plantar incision-induced drop of the noxious heat threshold in the rat

AU - Füredi, Réka

AU - Bölcskei, K.

AU - Szolcsányi, J.

AU - Pethő, G.

PY - 2010/2

Y1 - 2010/2

N2 - Aims: Previously 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 methods: Heat hyperalgesia was assessed by measuring the behavioural noxious heat threshold in conscious rats employing an increasing-temperature water bath. Key findings: The heat threshold drop evoked by a mild heat injury and measured 10min afterwards was reduced by intraplantarly applied HOE 140, a bradykinin B2 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-Arg10]-HOE 140, a bradykinin B1 receptor antagonist, L-NOARG, TNP-ATP and the TRPV1 receptor antagonist SB-366791. Significance: Only 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 B2 and B1 bradykinin receptor, P2X purinoceptors, TRPV1 receptor, nitric oxide synthase and lipoxygenase(s) are involved in at least one of these hyperalgesia models.

AB - Aims: Previously 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 methods: Heat hyperalgesia was assessed by measuring the behavioural noxious heat threshold in conscious rats employing an increasing-temperature water bath. Key findings: The heat threshold drop evoked by a mild heat injury and measured 10min afterwards was reduced by intraplantarly applied HOE 140, a bradykinin B2 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-Arg10]-HOE 140, a bradykinin B1 receptor antagonist, L-NOARG, TNP-ATP and the TRPV1 receptor antagonist SB-366791. Significance: Only 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 B2 and B1 bradykinin receptor, P2X purinoceptors, TRPV1 receptor, nitric oxide synthase and lipoxygenase(s) are involved in at least one of these hyperalgesia models.

KW - Heat hyperalgesia

KW - Heat injury

KW - Inflammatory mediators

KW - Noxious heat threshold

KW - Plantar incision

KW - TRPV1 receptor

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