ChloroquineV1, Istex, Corpus, bibRecord, 001A89

The pharmacology of arachidonic acid-induced rat paw edema

Identifieur interne : 001A89 ( Istex/Corpus ); précédent : 001A88; suivant : 001A90

The pharmacology of arachidonic acid-induced rat paw edema

Auteurs : M. J. Dimartino ; G. K. Campbell Jr. ; C. E. Wolff ; N. Hanna

Source :

Agents and Actions [ 0065-4299 ] ; 1987-08-01.

RBID : ISTEX:B1349A26653C38C4BE233854C07CBEFA8A71DE4E

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:

https://api.istex.fr/ark:/67375/1BB-6CGF476Z-6/fulltext.pdf

DOI: 10.1007/BF01966498

Links to Exploration step

ISTEX:B1349A26653C38C4BE233854C07CBEFA8A71DE4E

Le document en format XML

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<Para>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.</Para>
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<abstract 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.</abstract>
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The pharmacology of arachidonic acid-induced rat paw edema

The pharmacology of arachidonic acid-induced rat paw edema

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