The circulatory abnormalities typical of sepsis may depress the gut's normal barrier function, allowing translocation of bacteria and endotoxin into the systemic circulation (possibly via lymphatics, rather than the portal vein) and extending the septic response [64-67]. This is supported by animal models of sepsis, as well as a prospective cohort study that found that increased intestinal permeability (determined from the urinary excretion of orally administered lactulose and mannose) was predictive of the development of multiple organ dysfunction syndrome [68].