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Alanyl‐glutamine‐supplemented parenteral nutrition prevents intestinal ischemia‐reperfusion injury in rats
Author(s) -
Tazuke Y,
Wasa M,
Shimizu Y,
Wang HS,
Okada A
Publication year - 2003
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607103027002110
Subject(s) - glutamine , medicine , ischemia , intestinal mucosa , endocrinology , duodenum , pathogenesis , superior mesenteric artery , intestinal ischemia , reperfusion injury , gastroenterology , biochemistry , chemistry , amino acid
BACKGROUND: Intestinal ischemia‐reperfusion (I/R) injury plays an important role in the pathogenesis of systemic inflammation and multiple‐organ failure. We studied whether glutamine, the primary fuel of the small intestine, prevents intestinal mucosal damage after intestinal I/R in rats. METHODS: Rats were randomly divided into 4 groups: a sham‐standard amino acid (SAA) group (n = 8); a sham‐glutamine (Gln) group (n = 8); an I/R‐SAA group (n = 10); and an I/R‐Gln group (n = 9). Alanyl‐glutamine solution was produced by replacing 36% of the total amino acid nitrogen with Gln. The superior mesenteric artery was ligated. After 60 minutes of ischemia, reperfusion was initiated and infusion was started. After 24‐hour reperfusion, the intestinal segment was removed for morphological and biochemical analysis, and blood samples were drawn from the portal vein. Fluorescein isothiocyanate‐conjugated dextran 70,000 (FITC‐dextran) was infused into the duodenum 2 hours before animal death. RESULTS: In the I/R‐SAA group, extensive epithelial sloughing and mucosal ulceration of villous tips were observed, whereas these findings did not occur in the I/R‐Gln group. Mucosal wet weight, DNA, and protein content decreased significantly in the I/R‐SAA group compared with the sham‐SAA group and increased significantly in the I/R‐Gln group compared with the I/R‐SAA group. Plasma FITC‐dextran significantly increased in the I/R‐SAA group compared with the sham‐SAA group, but the plasma level in the I/R‐Gln group was comparable with that of each sham group. Mucosal glutaminase activity significantly increased in both the I/R‐SAA and I/R‐Gln groups compared with the sham‐SAA and sham‐Gln groups, respectively. CONCLUSIONS: Alanyl‐glutamine protects against morphologic and functional mucosal injury after intestinal I/R in rats.