The pharmacology of arachidonic acid-induced rat paw edema
Identifieur interne : 003332 ( Main/Exploration ); précédent : 003331; suivant : 003333The 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 :
- Agents and Actions [ 0065-4299 ] ; 1987-08-01.
English descriptors
- Teeft :
- Antiinflammatory, Antiinflammatory activity, Arachidonate metabolism, Arachidonic, Arachidonic acid, Arachidonic acid injection, Arachidonic acid metabolism, Carbonate buffer, Corticosteroid, Cyclooxygenase, Cyclooxygenase inhibitors, Dual inhibitors, Edema, Inflammation, Inhibitor, Lewis rats, Lipoxygenase, Lipoxygenase inhibitors, Lipoxygenase pathways, Mast cell mediator release, Meclofenamic acid, Mediator, Metabolism, Rheumatoid arthritis, Selective cyclooxygenase inhibitors.
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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Le document en format XML
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<front><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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