Premium
A POSSIBLE MODULATORY ROLE FOR PROSTACYCLIN (PGI 2 ) IN IgG a ‐INDUCED RELEASE OF SLOW‐REACTING SUBSTANCE OF ANAPHYLAXIS IN RATS
Author(s) -
BURKA J.F.,
GARLAND L.G.
Publication year - 1977
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.1476-5381.1977.tb07564.x
Subject(s) - microgram , prostacyclin , chemistry , ovalbumin , prostaglandin , ed50 , chronotropic , pharmacology , isoprenaline , in vivo , thromboxane a2 , endocrinology , medicine , antigen , in vitro , immunology , biochemistry , biology , receptor , heart rate , microbiology and biotechnology , stimulation , blood pressure
Antigen challenge in vivo of rat peritoneal cells (enriched with monocytes and polymorphonuclear leucocytes) passively sensitized 2 h previously with homologous antibody of the IgG a class released large amounts of slow‐reacting substance of anaphylaxis (SRS‐A, 1739 ± 59 u/ml) into the peritoneal fluid. This reaction was strongly inhibited by prostacyclin (PGI 2 , ED 50 = 0.5 μg/kg i.p.) and by isoprenaline (ED 50 = 0.2 μg/kg i.p.) but prostaglandins E 1 , E 2 and 6‐oxo‐prostaglandin F 1α were only weak inhibitors. Indomethacin (10 mg/kg, orally) augmented by 30% the release of SRS‐A, whereas thromboxane B 2 (50 μg/kg i.p.) had no effect. Lowering the antigen (ovalbumin) dosage from 400 μg/ml to 10 μg/ml reduced the control release of SRS‐A by 70% and increased the inhibitory effect of prostaglandins I 2 , E 1 and isoprenaline. Augmentation of release by indomethacin remained unchanged. These preliminary data suggested that endogenous prostacyclin may modulate the anaphylactic release of SRS‐A from rat peritoneal cells.