Abstract
428 ABSTRACT. The goal of this study was to characterize the importance of splanchnic viscera in liver ischemic reperfusion injury and to enhance the tolerance of liver to warm ischemia injury with portosystemic shunt. METHODS: The hepatic blood flow of male Sprague Dawley (SD) rats were subjected to 45 min, 60 min, 120 min, and 150 min liver warm ischemia with or without portosystemic shunt (splenic-caval shunt, SCS). The production and elimination of TNF, NF-kB activation, iNOS expression, and apoptosis were determined. RESULTS: All rats with 60 min warm ischemia without SCS died within one day (n=6). All rats with 120 min (n=8) liver warm ischemia in SCS group survived for over three days and 6 of them for over five days without significant histological changes of the liver. Serum TNF levels were significantly lower after liver reperfusion in SCS group compared to the rats with ischemia without SCS. Administration of LPS (1mg/kg, p.v.) induced a higher mortality rate (all rats died in one day, n=5), an earlier peak time (45 min vs 90 min after injection) and a higher concentration of serum rat TNF (465 pg/ml vs 240 pg/ml) in rats with liver ischemia and than in sham operating rats. The ability to eliminate huTNF was significantly reduced in the rats with long-term preserved liver (in cold Euro-Collin's solution for 16 hr) compared with short-term preserved and naive liver. iNOS expression and NF-kB activation were very strongly on the hepatocytes after liver warm ischemia with portosystemic shunt and compared to liver ischemia without portosytemic shunt. CONCLUSION: We conclude that the splanchnic viscera can contribute to liver ischemic reperfusion injury. Portosystemic shunt enhances the tolerance of liver to warm ischemia through activation of NF-kB and iNOS that prevents TNF a induced apoptosis.
Published Version
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