Synthesis of prostaglandins I₂ and E₂ by the canine gallbladder in vitro: Studies using a new incubation chamber

Using a specially designed incubation chamber, differential synthesis and the response to added arachidonic acid (25 mM) and L‐α‐phosphatidylcholine (LAP; 2mM) was quantified in gallbladders from male and female dogs. Prostaglandin I₂ (PGI₂) was the predominant prostanoid synthesized, and tissues from females produced much more PGI₂ under basal conditions than did gallbladders harvested from male dogs. Addition of arachidonic acid stimulated PGI₂ synthesis by almost 100 per cent. Arachidonate‐stimulated mucosal and serosal production of PGI₂ were (mean(s.e.m.)) comparable, 343(178) and 375(89) pg/cm²/min, respectively. Gallbladders from female animals synthesized significantly more PGI₂ than did tissue from males. Indomethacin inhibited PGI₂ synthesis in a dose–response manner; at 7 × 10⁻⁵ M, prostanoid synthesis was inhibited by >80 per cent. Arachidonic acid did not stimulate prostaglandin E₂ (PGE₂) production by gallbladder tissue. LAP similarly stimulated PGI₂ biosynthesis, but in contrast to the effect of arachidonic acid, the effect was significantly greater in the serosa than the mucosa, 355(107) and 213(59) pg/cm²/min, respectively. LAP also stimulated PGE₂ biosynthesis by the canine gallbladder in a pattern very similar to that of PGI₂. Based on the differences in response to the two agents added, we conclude that arachidonic acid and L‐α‐phosphatidylcholine stimulate prostaglandin biosynthesis via independent pathways. We advocate the use of the incubation chamber for the assessment of prostanoid biosynthesis by the gallbladder in vitro.