Forty dogs were divided randomly into four groups. The portal circulation was reduced to 50%—60% for one hour by partially occluding the superior mesenteric artery (SMA) for the purpose of determining the relationship between the reperfusion injury, bacterial translocation, and multiple system organ failure. Escherichia coli 0111 B4 (1 x 1010/kg) was fed to each animal 12 hours before operation. Group I constituted the controls, in which a sham operation was done. The experimental procedure was completed in all the animals of the other three groups. The group-II animals received no further manipulation. Rubia yunnanensis, an antioxidant, was given to the animals in group III. Amikacin was given to the animals in group IV. The results showed that the animals in group II developed bacteremia, hypoxemia, and hypotension compared with the animals in group I. The levels of superoxide dismutase (SOD) in whole blood were markedly lowered in group-II animals, with malondialdehyde (MDA) values significantly elevated after reperfusion when compared with group I. Plasma levels of anaphylatoxin C5a and thromboxane B2 (TXB2) were significantly raised in group-II animals beginning from reperfusion when compared with the animals in group I, group III, and group IV. Pathologic changes in the intestine, liver, and lung were marked only in the group-II animals, including acute necrosis of the intestinal mucosa, granulocyte infiltration, and bacterial invasion of the liver and lung. These results suggested that bowel ischemia and reperfusion may promote gut barrier failure and bacterial translocation, then contribute to the development of MSOF by allowing bacteria or endotoxin normally contained within the gut to reach the portal and systemic circulations, where it fuels the septic process. Oxygen free radicals, anaphylatoxin, and thromboxane may be potential factors in the development of gut barrier failure and MSOF.