Prostaglandin generation by human and guinea pig lung tissue: Comparison of parenchymal and airway responses

Effects of Arachidonic Acid, Monohydroxyeicosatetraenoic Acid and Prostaglandins on the Release of Mucous Glycoproteins from Human Airways In Vitro

“…PGE2, in contrast to all the other PG examined, consistently suppressed mucous release with a maximal effect at 1 ,uM. Indeed PGE2, the predominant PG produced by airways (12,14), was active at 0.01 ,uM (3.5 ng/ml), which is clearly within the physiologic range. In most organ systems, including the lung, AA is the predominant precursor of the naturally occurring PG (19,20).…”

“…in dogs in vivo is associated with increased bronchosecretory activity (11). PG are generated during human lung anaphylaxis (12)(13)(14) and mucous release is enhanced in anaphylaxis (2); therefore, it seemed appropriate to analyze the effect ofPG and other derivatives ofarachidonic acid (AA) on mucous glycoprotein release.…”

BAY u3405 an antagonist of thromboxane A2‐ and prostaglandin D2‐induced bronchoconstriction in the guinea‐pig

“…Challenge of sensitized human lung tissue in vitro, with antigen, causes the release of large amounts of PGD2 with smaller quantities of TXA2 (Steel et al, 1979;Schulman et al, 1981;1982). The exact site of release of these mediators in the lung remains unclear, although mast cells are known to release PGD2 in large quantities and macrophages and platelets release abundant amounts of TXA2 .…”

The Effect of Inhibitors of Arachidonic Acid Metabolism on Drug‐induced Contractions in Isolated Tracheal Smooth Muscle of the Pig

“…Hitherto a number of physiological and pathophysiological stimuli have been shown to cause the release of some of the above products of arachidonic acid. Pertinent to the present study however, are observations that some contracting drugs 0007-1188/82/010129-08 $01.00 liberate prostaglandins from guinea-pig (Orehek, Douglas & Bouhuys, 1975;Gryglewski, DembinskaKiec, Grodzinska & Panczenko, 1976) dog (Yamaguchi, Hitzig & Coburn, 1976;Anderson, Krzanowski, Polson & Szentivanyi, 1979a) and human (Steel, Platshon & Kaliner, 1979) airways. It has been argued that relaxant prostaglandins (PGE2) are produced in response to muscle contraction because inhibition of prostaglandin synthesis with indomethacin and aspirin leads to larger contractions in response to drugs (Orehek et al, 1975;Anderson, Krzanowski, Polson & Szentivanyi, 1979b;Krzanowski, Anderson, Polson & Szentivanyi, 1980).…”