Open AccessProtective effect of early enteral feeding on postburn impairment of liver function and its mechanism in rats
Author(s) -
Li Zhu
Publication year - 2000
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v6.i1.79
Subject(s) - medicine , enteral administration , albumin , splanchnic , endocrinology , liver function , bilirubin , vein , tumor necrosis factor alpha , basal (medicine) , blood flow , gastroenterology , parenteral nutrition , insulin
AIM:To study the protective effect of early enteral feeding (EEF) on the postburn impairment of liver function and its mechanism.METHODS:Wistar rats with 30% of total body surface area (TBSA) full-thickness burn were employed. The effects of EEF on the postburn changes of gastric intramucosal pH, endotoxin levels in portal vein, water contents of hepatic tissue, blood concentrations of tumor necrosis factor (TNF-alpha), plasma activities of alanine aminotransferase (ALT) and asparate aminotransferase (AST), as well as the blood contents of total (TB) and direct bilirubin (DB), total protein (TP) and albumin (ALB) were serially determined within 48h postburn.RESULTS:EEF could significantly improve gastric mucosal acidosis, reduce portal vein endotoxin level and water content of hepatic tissue, as well as plasma concentrations of TNF-alpha at all timepoints after severe burns (P < 0.01); postburn elevation of the plasma activities of ALT, AST and the contents of TB, DB were effectively prevented, whereas the plasma concentrations of TP and ALB were markedly increased 24h and 48h posturn in EEF group compared with that of the burn without EEF group (P < 0.01 ).CONCLUSION:EEF has significant beneficial effects on the improvement of hepatic function in rats after severe burn, and is probably related with an increase in splanchnic blood flow, reduction of the absorption of gut-origin endotoxin and the consequent release of inflammatory mediators.