Gut luminal endotoxin reduces ischemia-reperfusion injury of the small gut in germ-free pigs.

Translocation of luminal bacteria and their products through the intestinal mucosa during ischemia-reperfusion (I/R) may modify I/R injury. To test this hypothesis, 16 germ-free pigs were studied prior to and after clamping the superior mesenteric artery (SMA) and 12 pigs served as controls. Nine pigs in the I/R and 5 in the control group received endotoxin intragastrically, 60 min before baseline. Gut absorption of an inert indicator (polyethyleneglycol [PEG] 3350), gut intraluminal PCO 2 (tonometry), and systemic and regional hemodynamic variables were measured up to 4 h after baseline. Gut blood flow was stopped during clamping, some reactive hyperemia occurred up to 30 min after declamping in the I/R groups, independently of prior endotoxin administration. Gut intraluminal-arterial PCO 2 gradients were elevated in I/R versus control groups during I and for some time during R, prior endotoxin had no effect. However, in controls without and with luminal endotoxin, PEG urinary excretion, as percentage of the dose administered, was 0.12 ± 0.12 and 0.17 ± 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, respectively (P < 0.001). The data suggest that gut luminal endotoxin ameliorates I/R injury of the gut wall in germ-free pigs, without altering changes in gut perfusion adequacy and systemic hemodynamics.