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RELEASE OF MEDIATORS OF ANAPHYLAXIS: INHIBITION OF PROSTAGLANDIN SYNTHESIS AND THE MODIFICATION OF RELEASE OF SLOW REACTING SUBSTANCE OF ANAPHYLAXIS AND HISTAMINE
Author(s) -
ENGINEER DINAZ M.,
NIEDERHAUSER U.,
PIPER PRISCILLA J.,
SIROIS P.
Publication year - 1978
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1978.tb07006.x
Subject(s) - histamine , microgram , chemistry , prostaglandin , anaphylaxis , pharmacology , cromolyn sodium , liberation , ketoprofen , allergy , medicine , chromatography , immunology , biochemistry , in vitro , asthma
1 When isolated perfused lungs from sensitized guinea‐pigs were challenged with antigen, histamine, slow reacting substance of anaphylaxis (SRS‐A) and prostaglandin‐like substances were released into the effluent. 2 Treatment of the lungs before and during challenge with indomethacin (0.5–10 μg/ml), sodium aspirin (1–10 μg/ml), sodium meclofenamate (0.1–1 μg/ml) or ketoprofen (0.5–5 μg/ml) inhibited the release of prostaglandins while increasing the output of histamine and SRS‐A between three‐and five‐fold. 3 Diethylcarbamazine (0.2–1 mg/ml) reduced the release of SRS‐A and histamine but increased the amount of prostaglandin‐like substances produced. 4 Eicosatetraynoic acid (10 μg/ml) inhibited formation of prostaglandins but did not modify release of histamine and SRS‐A. 5 The results with non‐steroid anti‐inflammatory drugs and diethylcarbamazine suggest that prostaglandins, or some other product of the cyclo‐oxygenase system, depress the anaphylactic release of SRS‐A and histamine.