The role of prostaglandin I2 and biliary lipids during evolving cholecystitis in the rabbit

Acute cholecystitis increases gallbladder prostanoid synthesis. The percent study examined the hypothesis that increased endogenous gallbladder release of prostaglandin I2 (PGI2) after bile duct ligation is caused by both increased ductal pressure and altered biliary lipids.

Prostanoid release, biliary lipids, and in vitro fluid absorption of sham gallbladders were compared with those of gallbladders in which acute cholecystitis was induced after common bile duct ligation for 6, 24, and 72 hours.

Bile duct ligation for 6, 24, and 72 hours increased gallbladder PGI2 release twofold and increased gallbladder bile levels of lysolecithin and taurine-conjugated bile acids fivefold compared with sham groups (P < 0.05). In vitro gallbladder fluid absorption was decreased by 50% or more in the 6-, 24-, and 72-hour bile duct-ligated groups (P < 0.05) but was reversed by indomethacin only in the 6-hour ligated group.

Decreased gallbladder fluid absorption following bile duct ligation for 6 hours was caused by increased gallbladder release of PGI2. Decreased gallbladder fluid absorption following bile duct ligation for 24 and 72 hours was not a prostanoid-mediated process (not reversed by indomethacin) but was associated with increased bile levels of proinflammatory biliary lipids.