Differential effect of cyclo-oxygenase inhibition on antigen- and ionophore-induced release of slow reacting substance from fragmented guinea-pig lung.
The nonsteroidal anti-inflammatory drugs (NSAID) indomethacin and mefenamic acid, at concentrations ranging from 3 microM to 18 microM, enhanced antigen-induced slow reacting substance of anaphylaxis (SRS-A) release from sensitized fragmented guinea-pig lung. In contrast, these agents had no effect on SRS-A release from nonsensitized guinea-pig lung induced by several concentrations of the calcium ionophore, A23187. Neither increasing preincubation time with the NSAID nor the use of sensitized tissue resulted in an enhancement of A23187-induced SRS-A release by indomethacin. NSAID did not alter histamine release by either stimulus. These results suggest that antigen and A23187 induce SRS-A release from different sources or by different mechanisms in guinea-pig lung.
D015121:6-Ketoprostaglandin F1 alpha / Q000494:pharmacology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000941:Antigens / Q000276:immunology*; D000001:Calcimycin / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors; D011464:Epoprostenol / Q000096:biosynthesis; D005110:Extracellular Space / Q000378:metabolism; D006168:Guinea Pigs; D006632:Histamine / Q000378:metabolism; D066298:In Vitro Techniques; D007476:Ionophores / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008528:Mefenamic Acid / Q000494:pharmacology; D013189:SRS-A / Q000378:metabolism*; D013929:Thromboxane B2 / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000941:Antigens; D016861:Cyclooxygenase Inhibitors; D007476:Ionophores; D013189:SRS-A; D008528:Mefenamic Acid; D000001:Calcimycin; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D006632:Histamine; D011464:Epoprostenol