Endogenous pancreatic prostaglandin production in control and obstructive jaundice was investigated using isolated and perfused dog pancreas. In both groups, spontaneous production of prostaglandin E2 and prostaglandin I2 was recorded, and the levels did not change in both groups. The production of both prostaglandins in jaundice, however, was higher than that in the control on stimulation by 8 x 10(-11) mol of cholecystokinin-octapeptide. Amylase release with cholecystokinin-octapeptide at an amount of 8 x 10(-11) mol in jaundice was higher than in the control. The amylase release in both groups, however, showed further elevation on indomethacin pretreatment. On incubation of pancreatic dispersed cells in both groups, prostaglandin production in jaundiced cells was higher than that in control cells. These data showed that enhanced endogenous prostaglandin in obstructive jaundice might be caused by the characteristic change of pancreatic cells, which increased susceptibility to cholecystokinin-octapeptide because of long-term exposure to abnormal blood components, and enhanced prostaglandins might act as a cytoprotector of acinar cells in the pancreas damaged by cholecystokinin-octapeptide administration.