1984
DOI: 10.1111/j.1476-5381.1984.tb16484.x
|View full text |Cite
|
Sign up to set email alerts
|

Differential effect of cyclo‐oxygenase inhibition on antigen‐ and ionophore‐induced release of slow reacting substance from fragmented guinea‐pig lung

Abstract: The nonsteroidal anti‐inflammatory drugs (NSAID) indomethacin and mefenamic acid, at concentrations ranging from 3 μM to 18 μM, 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 en… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
2
0

Year Published

1985
1985
1993
1993

Publication Types

Select...
5
1

Relationship

0
6

Authors

Journals

citations
Cited by 10 publications
(2 citation statements)
references
References 21 publications
0
2
0
Order By: Relevance
“…The reason for the inability of NZ-107 to inhibit A23 187-induced SRS-A (or histamine) release is not clear but may be related to the fact that antigen-and A23187-induced SRS-A release occurs at different sites by different mechanisms in guinea-pig lung tissue. Antigen-induced SRS-A release is usually dependent upon mast cell activation (Krell & Kusner 1984), whereas that of A23 187 occurs not only in broncho-alveolar macrobages (Sirois 1980) but also in the pulmonary arteries $eisch & Haisch 1982). However, a lipoxygenase inhibitor, NJDGA, inhibited both antigen-and A231 87-induced SRS-A From these results, it is possible that NZ-107 blocked the release of arachidonic acid after antigen-antibody binding or that NZ-107 selectively inhibited the lipoxygenase pathway activated by antigen.…”
Section: Discussionmentioning
confidence: 99%
“…The reason for the inability of NZ-107 to inhibit A23 187-induced SRS-A (or histamine) release is not clear but may be related to the fact that antigen-and A23187-induced SRS-A release occurs at different sites by different mechanisms in guinea-pig lung tissue. Antigen-induced SRS-A release is usually dependent upon mast cell activation (Krell & Kusner 1984), whereas that of A23 187 occurs not only in broncho-alveolar macrobages (Sirois 1980) but also in the pulmonary arteries $eisch & Haisch 1982). However, a lipoxygenase inhibitor, NJDGA, inhibited both antigen-and A231 87-induced SRS-A From these results, it is possible that NZ-107 blocked the release of arachidonic acid after antigen-antibody binding or that NZ-107 selectively inhibited the lipoxygenase pathway activated by antigen.…”
Section: Discussionmentioning
confidence: 99%
“…They are synthesized de novo on exposure to immunological or non-immunological stimuli [68,69]. SRS-A is a major mediator released during guinea pig anaphylaxis and the guinea pig model has been used extensively in the study of pulmonary anaphylaxis both in vivo and in vitro [70][71][72][73][74]. SRS-A is released from the human lung mast cells on antigen challenge.…”
Section: B Mediators Released From Lung (I) Histaminementioning
confidence: 99%