The pharmacology of arachidonic acid-induced rat paw edema

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)...

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Bibliographic Details
Published inAgents and actions Vol. 21; no. 3-4; p. 303
Main Authors DiMartino, M J, Campbell, Jr, G K, Wolff, C E, Hanna, N
Format Journal Article
LanguageEnglish
Published Switzerland 01.08.1987
Subjects
Adrenal Cortex Hormones - pharmacology
Animals
Anti-Inflammatory Agents - pharmacology
Arachidonic Acid
Arachidonic Acids - pharmacology
Cyclooxygenase Inhibitors
Edema - chemically induced
Edema - prevention & control
Lipoxygenase Inhibitors
Male
Rats
Rats, Inbred Lew
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Summary: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.
ISSN:0065-4299
DOI:10.1007/bf01966498