Indomethacin and the Gastric Mucosal Blood Flow Changes of Sepsis

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Abstract
Evidently, sepsis results in increased gastric mucosal blood flow (GBF). To investigate the possible role of prostaglandins in mediating this response, 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 (7 sepsis controls, 7 indomethacin controls and 8 experimental [indomethacin pretreated sepsis]). Sepsis was produced in piglets by bolus i.v. injection of 109 live Escherichia coli followed by an infusion of 109 E. coli/h. Cardiac output (CO) 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 per 100 g tissue). There were significant (P < 0.05) increases in gastric mucosal blood flow to the fundus (+47%), corpus (+50%) and antrum (+101%) at 15 min following the onset of E. coli infusion. At 135 min, the increase was only significant in the antrum. GMBF did not change in the indomethacin control or indomethacin pretreated sepsis groups. GMBF was demonstrated 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 increased GMBF may be a prostaglandin mediated response.
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