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The pharmacology of arachidonic acid-induced rat paw edema

Identifieur interne : 003332 ( Main/Exploration ); précédent : 003331; suivant : 003333

The pharmacology of arachidonic acid-induced rat paw edema

Auteurs : M. J. Dimartino [États-Unis] ; G. K. Campbell Jr. [États-Unis] ; C. E. Wolff [États-Unis] ; N. Hanna [États-Unis]

Source :

RBID : ISTEX:B1349A26653C38C4BE233854C07CBEFA8A71DE4E

English descriptors

Abstract

Abstract: Arachidonic acid (AA) injected into hindpaws of Lewis rats produces a severe edematous response. Treatment with corticosteroids (dexamethasone, prednisolone), dual inhibitors of arachidonate metabolism (phenidone, SK & F 86002), anti-histamine/serotonin agents (chlorpheniramine, cyproheptadine) and a gold compound (auranofin) inhibited AA-induced edema. In contrast, administration of high doses of cyclooxygenase inhibitors (indomethacin, piroxicam, naproxen, ibuprofen, meclofenamic acid and tiflamizole) did not affect AA-induced hind paw edema. The involvement of lipoxygenase products and mast cell mediators in the edematous response to arachidonic acid render this model potentially useful for studying antiinflammatory agents with a mechanism of action different from that of cyclooxygenase inhibitors.

Url:
DOI: 10.1007/BF01966498


Affiliations:


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<div type="abstract" xml:lang="en">Abstract: Arachidonic acid (AA) injected into hindpaws of Lewis rats produces a severe edematous response. Treatment with corticosteroids (dexamethasone, prednisolone), dual inhibitors of arachidonate metabolism (phenidone, SK & F 86002), anti-histamine/serotonin agents (chlorpheniramine, cyproheptadine) and a gold compound (auranofin) inhibited AA-induced edema. In contrast, administration of high doses of cyclooxygenase inhibitors (indomethacin, piroxicam, naproxen, ibuprofen, meclofenamic acid and tiflamizole) did not affect AA-induced hind paw edema. The involvement of lipoxygenase products and mast cell mediators in the edematous response to arachidonic acid render this model potentially useful for studying antiinflammatory agents with a mechanism of action different from that of cyclooxygenase inhibitors.</div>
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