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Short bowel syndrome is an important complication of surgery for resection of a portion of the small intestine. Intestinal Na+ absorption may contribute to the pathophysiology. We hypothesized that intestinal Na+ absorption inhibits the inflammatory response and sought to test this hypothesis in animals that did or did not have diminished Na+ absorption and developed a model for the syndrome in which animals received an endotoxin intravenously to induce intestinal injury. We determined whether intestinal Na+ absorption inhibits the systemic inflammatory response to an endotoxin insult and whether the Na+ channel ATP-sensitive 2 (Na(+)-K(+)-ATPase) protects against endotoxemic injury. A 37.5% resection of the small bowel was performed in young swine, and animals were tested to determine intestinal Na+ absorption. Endotoxemia was induced in these animals 4 wk later by intravenous endotoxin. Intestinal injury was induced to initiate the syndrome. Animals were treated with an AT(1) receptor blocker, Na(+)-K(+)-ATPase antireceptor
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