Gomes, J. C.Basso, S. V.2014-05-272014-05-271986-01-01Agents and Actions, v. 18, n. 1-2, p. 191-193, 1986.0065-4299http://hdl.handle.net/11449/63758Histamine 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 48/80.191-193eng7 [3 (4 acetyl 3 hydroxy 2 propylphenoxy) 2 hydroxypropoxy] 4 oxo 8 propyl 4h 1 benzopyran 2 carboxylic acidacetylsalicylic acidcompound 48-80indometacinnonsteroid antiinflammatory agentphenylbutazonepiroxicamanaphylaxisanimal celldrug efficacydrug potentiationguinea pighearthistamine releasein vitro studynonhumanAnaphylaxisAnimalAnti-Inflammatory AgentsArachidonic AcidArachidonic AcidsChromonesGuinea PigsHistamine ReleaseIn VitroMyocardiump-Methoxy-N-methylphenethylamineSupport, Non-U.S. Gov'tArtigo10.1007/BF01988018Acesso restrito2-s2.0-0022577296