Gut luminal endotoxin reduces ischemia-reperfusion injury of the small gutin germ-free pigs

Translocation of luminal bacteria and their products through the intestinal mucosa during ischemia-reperfusion (IIR) may modify I/R injury. To test th is hypothesis, 16 germ-free pigs were studied prior to and after clamping t he superior mesenteric artery (SMA) and 12 pigs served as controls. Nine pi gs in the I/R and 5 in the control group received endotoxin intragastricall y, 60 min before baseline. Gut absorption of an inert indicator (polyethyle neglycol [PEG] 3350), gut intraluminal PCO2 (tonometry), and systemic and r egional hemodynamic variables were measured up to 4 h after baseline. Gut b lood flow was stopped during clamping, some reactive hyperemia occurred up to 30 min after declamping in the I/R groups, independently of prior endoto xin administration. Gut intraluminal-arterial PCO2 gradients were elevated in I/R versus control groups during I and for some time during R, prior end otoxin had no effect. However, in controls without and with luminal endotox in, PEG urinary excretion, as percentage of the dose administered, was 0.12 +/- 0.12 and 0.07 +/- 0.07, respectively, while it measured 1.82 +/- 0.70 in the I/R group and 0.55 +/- 0.37% in the I/R and endotoxin groups, respec tively (P < 0.001.). The data suggest that gut luminal endotoxin ameliorate s I/R injury of the gut wall in germ-free pigs, without altering changes in gut perfusion adequacy and systemic hemodynamics.