Mechanisms contributing to the vaso-active effects of prilocaine in human skin

D. J. Newton, E. L. Sur, F. Khan, G. A. McLeod, J. J. F. Belch

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    We investigated the roles of the endothelial nitric oxide and cyclo-oxygenase pathways in mediating the vasoactivity of prilocaine in the skin. We injected prilocaine 1% intradermally into forearm skin of 10 healthy, male subjects. Nitric oxide synthesis was inhibited at a second site by co-injecting prilocaine with l-NAME 1%. We then repeated the injections while blocking the cyclo-oxygenase pathway with aspirin (4 x 600 mg). We measured blood flow responses to the injections using laser Doppler imaging. We found that, after the traumatic effects of injection had subsided, l-NAME reduced the vascular response to prilocaine by a third (p = 0.012), indicating an influence specifically on the drug response. Aspirin had no effect on the response (p = 0.588). We conclude that the vasoactive effects of prilocaine in human skin are mediated partly through the release of endothelial nitric oxide and, although other mechanisms might also be involved, the cyclo-oxygenase pathway does not appear to play a role.
    Original languageEnglish
    Pages (from-to)6-10
    Number of pages5
    JournalAnaesthesia
    Volume58
    Issue number1
    DOIs
    Publication statusPublished - 2003

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    Prilocaine
    Prostaglandin-Endoperoxide Synthases
    Skin
    Nitric Oxide
    Aspirin
    Injections
    Forearm
    Blood Vessels
    Healthy Volunteers
    Lasers
    Pharmaceutical Preparations

    Cite this

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    title = "Mechanisms contributing to the vaso-active effects of prilocaine in human skin",
    abstract = "We investigated the roles of the endothelial nitric oxide and cyclo-oxygenase pathways in mediating the vasoactivity of prilocaine in the skin. We injected prilocaine 1{\%} intradermally into forearm skin of 10 healthy, male subjects. Nitric oxide synthesis was inhibited at a second site by co-injecting prilocaine with l-NAME 1{\%}. We then repeated the injections while blocking the cyclo-oxygenase pathway with aspirin (4 x 600 mg). We measured blood flow responses to the injections using laser Doppler imaging. We found that, after the traumatic effects of injection had subsided, l-NAME reduced the vascular response to prilocaine by a third (p = 0.012), indicating an influence specifically on the drug response. Aspirin had no effect on the response (p = 0.588). We conclude that the vasoactive effects of prilocaine in human skin are mediated partly through the release of endothelial nitric oxide and, although other mechanisms might also be involved, the cyclo-oxygenase pathway does not appear to play a role.",
    author = "Newton, {D. J.} and Sur, {E. L.} and F. Khan and McLeod, {G. A.} and Belch, {J. J. F.}",
    year = "2003",
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    language = "English",
    volume = "58",
    pages = "6--10",
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    Mechanisms contributing to the vaso-active effects of prilocaine in human skin. / Newton, D. J.; Sur, E. L.; Khan, F.; McLeod, G. A.; Belch, J. J. F.

    In: Anaesthesia, Vol. 58, No. 1, 2003, p. 6-10.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Mechanisms contributing to the vaso-active effects of prilocaine in human skin

    AU - Newton, D. J.

    AU - Sur, E. L.

    AU - Khan, F.

    AU - McLeod, G. A.

    AU - Belch, J. J. F.

    PY - 2003

    Y1 - 2003

    N2 - We investigated the roles of the endothelial nitric oxide and cyclo-oxygenase pathways in mediating the vasoactivity of prilocaine in the skin. We injected prilocaine 1% intradermally into forearm skin of 10 healthy, male subjects. Nitric oxide synthesis was inhibited at a second site by co-injecting prilocaine with l-NAME 1%. We then repeated the injections while blocking the cyclo-oxygenase pathway with aspirin (4 x 600 mg). We measured blood flow responses to the injections using laser Doppler imaging. We found that, after the traumatic effects of injection had subsided, l-NAME reduced the vascular response to prilocaine by a third (p = 0.012), indicating an influence specifically on the drug response. Aspirin had no effect on the response (p = 0.588). We conclude that the vasoactive effects of prilocaine in human skin are mediated partly through the release of endothelial nitric oxide and, although other mechanisms might also be involved, the cyclo-oxygenase pathway does not appear to play a role.

    AB - We investigated the roles of the endothelial nitric oxide and cyclo-oxygenase pathways in mediating the vasoactivity of prilocaine in the skin. We injected prilocaine 1% intradermally into forearm skin of 10 healthy, male subjects. Nitric oxide synthesis was inhibited at a second site by co-injecting prilocaine with l-NAME 1%. We then repeated the injections while blocking the cyclo-oxygenase pathway with aspirin (4 x 600 mg). We measured blood flow responses to the injections using laser Doppler imaging. We found that, after the traumatic effects of injection had subsided, l-NAME reduced the vascular response to prilocaine by a third (p = 0.012), indicating an influence specifically on the drug response. Aspirin had no effect on the response (p = 0.588). We conclude that the vasoactive effects of prilocaine in human skin are mediated partly through the release of endothelial nitric oxide and, although other mechanisms might also be involved, the cyclo-oxygenase pathway does not appear to play a role.

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    JO - Anaesthesia

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