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EFFECT OF SULPHASALAZINE ON PULMONARY INACTIVATION OF PROSTAGLANDIN F 2α IN THE PIG
Author(s) -
HELLEWELL P.G.,
PEARSON J.D.
Publication year - 1982
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.1476-5381.1982.tb09223.x
Subject(s) - prostaglandin , chemistry , extracellular , pharmacology , prostaglandin d2 , ic50 , perfusion , metabolism , ficoll , albumin , biochemistry , medicine , in vitro , biology , peripheral blood mononuclear cell
1 The metabolism of prostaglandin F 2α (PGF 2α ) 15 nM in 100,000 g supernatant fractions from piglet lung homogenates was inhibited by sulphasalazine with an IC 50 value of 25 μ m . 2 The piglet isolated lung perfused with Krebs solution, containing either albumin or Ficoll 70 to prevent oedema and vascular damage, efficiently metabolized PGF 2α given as a bolus injection (1 ng in 0.1 ml; 30 nM). 3 In Krebs solution containing Ficoll 70, sulphasalazine inhibited the pulmonary inactivation of PGF 2α in a dose‐dependent manner with an IC 50 value of 110 μ m . No inhibition of inactivation by sulphasalazine was found when the perfusion fluid contained albumin, which is known to bind this drug effectively. 4 Analysis of the separated efflux profiles for PGF 2α and its metabolites with reference to the dilution curve for an extracellular marker provided evidence that sulphasalazine inhibited PGF 2α uptake into lung cells. 5 We conclude that the effect of sulphasalazine on pulmonary prostaglandin inactivation is primarily due to inhibition of prostaglandin transport, and not to inhibition of prostaglandin metabolism.