Premium
Paf‐induced release of spasmogens from guinea‐pig lungs
Author(s) -
Jancar S.,
Thériault P.,
Lauzière M.,
Braquet P.,
Sirois P.
Publication year - 1989
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.1476-5381.1989.tb11795.x
Subject(s) - guinea pig , leukotriene , nordihydroguaiaretic acid , chemistry , bronchus , leukotriene d4 , pharmacology , leukotriene b4 , platelet activating factor , microgram , lung , lipoxygenase , medicine , endocrinology , biochemistry , respiratory disease , in vitro , enzyme , asthma , inflammation
1 The injection of platelet activating factor (Paf; 250 ng), leukotriene B 4 (LTB 4 ; 50 ng) and leukotriene D 4 (LTD 4 ; 10 ng) elicited contractions of strips of guinea‐pig trachea, bronchus and lung parenchyma. 2 When the effluent of perfused guinea‐pig lungs was superfused over strips of guinea‐pig trachea, bronchus and parenchyma, the intra‐arterial injection of Paf (250 ng) caused the release of spasmogen(s) which contracted all three tissues. 3 The infusion of indomethacin (10 μg ml −1 ) into the pulmonary artery and over the assay tissues inhibited the responses of the tissues to the effluent of the lungs stimulated by Paf (250 ng) and LTB 4 (50 ng). However, treating only the assay tissues with indomethacin (10 μg ml −1 ) did not block the contractile responses to the effluent of the lungs stimulated with LTB 4 or Paf. stimulated with Paf. 4 Pretreatment of the lungs with indomethacin (10 μg ml −1 ) or aspirin (30 μg ml −1 ) for 30 min, washing them out and suspending them over the assay tissues did not block the release of spasmogens elicited by Paf but appeared to inhibit the release of cyclo‐oxygenase products. 5 The infusion of two lipoxygenase inhibitors, nordihydroguaiaretic acid (NDGA; 1 μg ml −l ) and L‐655,240 (1 μg ml −1 ), into the pulmonary artery completely blocked the release of spasmogen(s) from the perfused lungs. 6 The slow reacting substance of anaphylaxis (SRS‐A) antagonist, FPL‐55712 (10 ng ml −1 ), did not block the responses of the tissues to the spasmogen(s) released by Paf. 7 The infusion of the Paf antagonist BN‐52021 (30 μg ml −1 ) into the pulmonary artery completely abolished the release of spasmogen(s) induced by Paf. 8 These data suggest that a lipoxygenase product, possibly LTB 4 , could be responsible for the spasmogenic activity released by the lungs following Paf stimulation. Cyclo‐oxygenase products released following Paf stimulation appear to result from the initial LTB 4 generation.