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One of its most frequent consequences is ileus, which can increase mortality. Animal models such as that induced by systemic administration of lipopolysaccharide (LPS) are useful to deeply evaluate this condition. The effects of sepsis on the gastrointestinal (GI) tract have been explored but, to our knowledge, in vivo studies showing the motor and histopathological consequences of endotoxemia in an integrated way are lacking. Our aim was to study in rats the effects of sepsis on GI motility, using radiographic methods, and to assess histological damage in several organs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Male rats were intraperitoneally injected with saline or <jats:italic>E.\u2009coli<\/jats:italic> LPS at 0.1, 1, or 5\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>. Barium sulfate was intragastrically administered, and X\u2010rays were performed 0\u201324\u2009h afterwards. Several organs were collected for organography, histopathology, and immunohistochemistry studies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>All LPS doses caused gastroparesia, whereas changes in intestinal motility were dose\u2010and time\u2010dependent, with an initial phase of hypermotility followed by paralytic ileus. Lung, liver, stomach, ileum, and colon (but not spleen or kidneys) were damaged, and density of neutrophils and activated M2 macrophages and expression of cyclooxygenase 2 were increased in the colon 24\u2009h after LPS 5\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Inferences<\/jats:title><jats:p>Using radiographic, noninvasive methods for the first time, we show that systemic LPS causes dose\u2010, time\u2010, and organ\u2010dependent GI motor effects. 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