Effect of non-steroidal anti-inflammatory drugs (NSAID) on the histamine release induced by compound 48/80 and cardiac anaphylaxis in guinea-pig isolated heart
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Data
1986-01-01
Autores
Gomes, J. C.
Basso, S. V.
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Resumo
Histamine release from guinea pig heart treated with compound 48/80 was potentiated by the cyclooxygenase inhibitors indomethacin and piroxicam but not by aspirin or phenylbutazone. This differential effect suggests that the potentiation is not merely due to an inhibition of prostaglandin synthesis. Piroxicam potentiated the histamine release induced by cardiac anaphylaxis whereas indomethacin reduced this effect. The SRS-A antagonist FPL 55712 inhibited histamine release induced by cardiac anaphylaxis, but not that evoked by compound 48/80, and also prevented the potentiation due to indomethacin and piroxicam. In total, these data suggest that the potentiation of histamine release by piroxicam and indomethacin is probably due to a diversion of arachidonic acid metabolism from the cyclooxygenase to the lipoxygenase pathways. The resulting lipoxygenase products may then regulate histamine release, with the secretion due to antigen being more sensitive to such modulation than that evoked by compound 48/80.
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7 [3 (4 acetyl 3 hydroxy 2 propylphenoxy) 2 hydroxypropoxy] 4 oxo 8 propyl 4h 1 benzopyran 2 carboxylic acid, acetylsalicylic acid, compound 48-80, indometacin, nonsteroid antiinflammatory agent, phenylbutazone, piroxicam, anaphylaxis, animal cell, drug efficacy, drug potentiation, guinea pig, heart, histamine release, in vitro study, nonhuman, Anaphylaxis, Animal, Anti-Inflammatory Agents, Arachidonic Acid, Arachidonic Acids, Chromones, Guinea Pigs, Histamine Release, In Vitro, Myocardium, p-Methoxy-N-methylphenethylamine, Support, Non-U.S. Gov't
Como citar
Agents and Actions, v. 18, n. 1-2, p. 191-193, 1986.