Abstract
BACKGROUND: It has been reported that glycine may protect donor small intestine against hypothermic ischemia before transplantation. This is consistent with the documented role of glycine as a natural cytoprotectant. OBJECTIVE: Using an in vivo rodent model, we sought to determine whether exposure to a 20% glycine solution reduces the extent of warm ischemia-reperfusion injury. METHODS: Wistar rats (n = 50) underwent laparotomy. A baseline group did not receive any further intervention. The remaining animals had cannulation of the aorta before the initiation of intestinal ischemia (30 minutes) followed by reperfusion (30 minutes). Using a factorial design, rats were randomized to receive local tissue perfusion with either normal saline or a 20% glycine solution during either the preischemia or the prereperfusion phase. Standardized segments of small intestine were removed at the end of the study period to determine the extent of ischemia-reperfusion injury. RESULTS: Perfusion with 20% glycine increased mucosal protein content (p < .05), increased mucosal DNA content (p < .05), reduced intestinal myeloperoxidase activity (p < .05), and maintained mucosal glutaminase activity. This was true regardless of whether glycine was administered during the preischemia phase or the prereperfusion phase. CONCLUSIONS: Local perfusion with 20% glycine can diminish warm ischemia-reperfusion injury to the rat small intestine in an in vivo model. The role of glycine supplementation should be evaluated in situations where hemodynamic instability may be responsible for breakdown in the gut barrier.
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