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); post-reperfusion treated with fructose 1-6 diphosphate (n = 7); and post-reperfusion 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. Post-reperfusion arterial pressure was significantly lower in the control rats (p less than 0.001) as well as when compared with the fructose 1-6 diphosphate groups (p less than 0.001). Significant increase in white blood cell counts occurred in the controls (p less than 0.001), whereas in the fructose 1-6 diphosphate groups white blood cell counts were no different from preischemic values. All control rats that died in less than 5 days had transmural intestinal necrosis, whereas in 3 of the controls that survived 5 days, partial intestinal necrosis was noted. Only one fructose 1-6 diphosphate-treated rat had partial intestinal necrosis. The overall 5-day survival was 100% for sham-operated rats, 93% for fructose 1-6 diphosphate-treated rats, and 21% for controls (fructose 1-6 diphosphate vs. controls, p less than 0.001; fructose 1-6 diphosphate vs. sham, NS). The results are discussed and explained in terms of the postulated mechanism based on the pharmacological properties of fructose 1-6 diphosphate.
journal_name
Gastroenterologyjournal_title
Gastroenterologyauthors
Sun JX,Farias LA,Markov AKdoi
10.1016/0016-5085(90)91299-lsubject
Has Abstractpub_date
1990-01-01 00:00:00pages
117-26issue
1eissn
0016-5085issn
1528-0012pii
0016-5085(90)91299-Ljournal_volume
98pub_type
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