Recent evidence suggests that sepsis results in increased gastric mucosal blood flow (GMBF). To investigate the possible role of prostaglandins in mediating this response, the GMBF was measured in the fundus, corpus, and antrum of pig stomachs with and without pretreatment with indomethacin, an inhibitor of prostaglandin synthesis, before and after the induction of bacteremia. The studies were done in 22 piglets (seven sepsis controls, seven indomethacin controls and eight experimental [indomethacin pretreated sepsis] ). Sepsis was produced in piglets by bolus intravenous injection of 10(9) live Escherichia coli followed by an infusion of 10(9) E. coli/hr. Cardiac output (C.O.) was measured by thermodilution. GMBF was measured by microsphere trapping. Following sacrifice, hyperemia was noted in the sepsis group but not in the other groups. GMBF was determined by standard techniques (expressed as ml/min/100 gm tissue). There were significant (p less than 0.05) increases in gastric mucosal blood flow to the fundus (+47%), corpus (+50%), and antrum (+101%) at 15 minutes following the onset of E. coli infusion. At 135 minutes, the increase was only significant in the antrum. GMBF, however, did not change in the indomethacin control or indomethacin pretreated sepsis groups. These data demonstrate GMBF in the stomach following sepsis. The changes were not present in the indomethacin control or in the indomethacin pretreated sepsis groups. Since indomethacin is an inhibitor of prostaglandin synthesis, the results suggest that the GMBF may be a prostaglandin mediated response.