Article
Effects of a preconditioning oral nutritional supplement (pONS) on pig livers after warm ischemia
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Published: | May 17, 2010 |
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Introduction: Polyphenolic constituents of Green tea (Camellia sinenesis) have been shown to be potent scavengers of reactive oxygen species. This study was designed to evaluate the effects of a preconditioning Oral Nutritional Supplement containing carbohydrates, glutamine, antioxidants and green tea extract on hepatic warm ischemia/reperfusion injury in pigs
Materials and methods: pONS (70 g/serving, Fresenius Kabi, Germany), dissolved in 250 ml tap water was given to pigs at 24, 12 and 2h before warm ischemia of the liver. A 4th dose was given 3h after reperfusion. Controls were given the same amount of cellulose with the same volume of water. All animals were treated with humane care and were fasted over night. Two hours after administration of the 3rd dose of pONS, both the portal vein and the hepatic artery were clamped for 40 min. At 0.5, 3, 6, and 8h after reperfusion, pulse rate (PR), mean arterial pressure (MAP), central venous pressure (CVP), portal venous flow (PVF), hepatic arterial flow (HAF), bile flow, and transaminases were measured. Liver tissue was taken 8h after reperfusion for histology (H&E) and immunohistochemistry (TNF-α, myeloperoxidase, caspase-3). Analysis of variance (ANOVA) or Mann-Whitney rank sum test was used as appropriate. Results are presented as mean ± SEM.
Results: PR, MAP, CVP, HAF, and PVF were comparable between the two groups. pONS significantly increased bile production at 8h after reperfusion. ALT and AST were significantly lower after pONS (35±3 vs. 49±3 at 6 hrs and 33±4 vs. 50±3 at 8 hrs for ALT and 57±13 vs. 112±38 at 8 hrs for AST). Histology showed more severe necrosis and neutrophil infiltration in controls. pONS significantly decreased the index of immunohistochemical expression for TNF-α, MPO, and caspase-3 (p<0.001).
Conclusion: pONS dose before and after tissue damage protects the liver from warm ischemia / reperfusion by decreasing oxidative stress, lipid peroxidation, apoptosis, and necrosis.