Abstract
Alterations in the gastric mucosal barrier, one of whose fundamental components is phosphatidylcholine (PC), may play an important role in the pathophysiology of erosive gastritis secondary to sepsis. Pentoxifylline (PTX) has been shown to reduce tissue damage in various experimental models of sepsis. The aim of this study was to investigate the effect of PTX on gastric mucosa PC synthesis, leukocyte infiltration, arachidonic acid-related metabolites, inflammation, oxidative stress, NO, CO, and somatostatin in a rat model of LPS-induced sepsis. Rats were administered LPS (10 mg/kg b.w.) intraperitoneally. After 30 min (early treatment group) or 120 min (late treatment group) of LPS administration, they were randomly divided into two groups that were intraperitoneally administered saline (5 mL/kg; LPS + Saline group) or PTX (45 mg/kg; 5 mL/kg; LPS + PTX group). Control rats received only saline instead of LPS and/or PTX. Two hours after saline or PTX administration (total of 150 or 240 min of procedure), animals were anesthetized, and then gastric lavage, gastric mucosa and plasma samples were obtained and kept frozen until determination. LPS-induced sepsis changed the gastric mucosal barrier by reducing its phospholipid content, PGI2, and somatostatin levels, as well as increasing MPO, TXB2, LTB4, PLA2, and MDA. Alterations may be mediated, at least in part, by modifications in the production of NO, CO, and cGMP content. PTX had a beneficial effect on gastric lesions secondary to sepsis by restoring PC production.