The relationship between the cause of postoperative major organ dysfunction and sepsis or endotoxemia was determined following hepatic surgery in 147 cirrhotic patients. Postoperative endogenous or exogenous endotoxemia induced high morbidity and mortality after surgery. The fact that postoperative endotoxemia was caused by long-term fasting suggested the presence of bacterial translocation. In experimental studies, metabolic alteration in the liver, skeletal muscle and gut was evaluated during sepsis which was induced by cecal ligation and puncture (CLP) in rats with thioacetamide-induced cirrhosis. The protein synthesis rate in vivo was measured by the flooding dose technique utilizing 14C-leucine. In particular, the protein synthesis rate in isolated enterocytes was determined by measuring incorporation of amino acid into protein during incubation for 30 min with 3H- phenylalanine in vitro. In cirrhotic rats, the protein synthesis rates and protein content of the liver, skeletal muscle and gut were lower than those in normal rats during sepsis. In addition, the mortality rate for cirrhotic rats was higher than for normal rats 24 hours after CLP. As nutritional supports, enteral nutrition (EN), pareteral nutrition (PN) or non-therapy (Non) were carried out following surgery. When EN was given during sepsis in cirrhotic rats, protein synthesis rate in the liver and gut was 89 ± 6, 83 ± 9%/day, respectively, which was significantly higher than in animals given PN or Non with improvement in the amino acid clearance rates: glutamine in the gut and alanine in the liver. Moreover, EN increased protein synthesis including secreted protein production in isolated enterocytes, and also inhibited the decrease in the number of enterocytes and protein content of the gut during sepsis, thus decreasing the mortality rate.
|Number of pages||6|
|Journal||The Japanese Journal of Gastroenterological Surgery|
|Publication status||Published - 1993|
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