Fructose 1–6 diphosphate prevents intestinal ischemic reperfusion injury and death in rats

Abstract This study of ischemic and postischemic reperfusion intestinal injury in rats evaluates the potential therapeutic value of fructose 1–6 diphosphate on the basis of its ability to enhance anaerobic carbohydrate metabolism during ischemia and to prevent additional tissue injury after reestablishing blood flow by inhibiting the neutrophils to produce oxygen free radicals. In pursuit of this goal, 28 rats were randomized into 4 groups: pretreated with fructose 1–6 diphosphate (n = 7); pretreated with glucose (n = 7); postreperfusion treated with fructose 1–6 diphosphate (n = 7); and postreperfusion treated with saline (n = 7). Five additional rats were sham operated. Following 30 min occlusion of the superior mesenteric artery, all rats received their respective treatments for 5 days. Postreperfusion arterial pressure was significantly lower in the control rats (p