Endotoxin level in ischemia–reperfusion injury in rats: Effect of glutamine pretreatment on endotoxin levels and gut morphology
Abstract
Objective
We aimed to investigate the effect of enteral glutamine (Gln) pretreatment on plasma endotoxin level and intestinal histopathologic changes during intestinal ischemia–reperfusion (I/R) injury in rats.
Methods
Intestinal I/R was induced by 60-min occlusion of the superior mesenteric artery followed by 60
min of reperfusion. Animals were pretreated with Gln by orogastric route for different periods and doses. To investigate the effects of gut decontamination on intestinal I/R injury, animals were pretreated with neomycin sulfate and erythromycin phosphate by orogastric route. In another series, dl-α-tocopherol hydrogen succinate was used to investigate the effects of vitamin E on intestinal I/R injury. Plasma endotoxin level was measured by the colorimetric “limulus amebocyte lysate” test. Intestinal mucosal injury was scored on a scale described by Chiu et al. (Archive in Surgery 1970;101:478–483).
Results
Intestinal I/R increased the plasma endotoxin level and worsened the histopathologic score significantly. Gln pretreatment (1
g/kg) for 4 d reduced the I/R-induced elevation of plasma endotoxin level. However, a significant improvement in histopathologic score could only be achieved when the pretreatment was given for 7 d. Antibiotic pretreatment lowered plasma endotoxin level without affecting the I/R-induced histopathologic changes, whereas vitamin E pretreatment affected plasma endotoxin level and histopathologic changes.
Conclusion
These results suggest a lack of association between plasma endotoxin level and intestinal histopathologic alterations in intestinal I/R.
Keywords: Intestinal ischemia–reperfusion, Glutamine, Endotoxin, Gut decontamination, Vitamin E
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This study was supported by a grant from TUBİTAK, the Scientific and Technological Research Council of Turkey (project 105S143 [SBAG-HD-35]).
PII: S0899-9007(09)00175-0
doi:10.1016/j.nut.2009.04.010
© 2010 Elsevier Inc. All rights reserved.
