Skeletal muscle catabolism is of the characteristics of postoperative protein metabolism. Postoperative nutritional management, therefore, should be aimed at preventing muscle catabolism. Few data are available to show how muscle protein metabolism is affected by the route of nutritional substrate intake. This study investigated the effects of the route of nutrient intake on postoperative protein metabolism. Wistar rats that had received gastrectomy were infused with a total parenteral nutrition solution by either the enteral or parenteral route. On the 3rd or 7th postoperative day (POD), ¹⁵N-glycine was infused for 18-24 hours by either route. Whole-body protein turnover (WPT), synthesis, and breakdown were determined by urinary ¹⁵N total nitrogen enrichment. Fractional protein biosynthesis rates (FSR) for skeletal muscle and wounds were calculated by analyzing ¹⁵N tissue enrichment. IgA-containing cells and height of the intestinal villi were determined histochemically. Urinary catecholamine excretion was mesured by liquid chromatography. In parenterally fed rats, WPT and breakdown did not differ significantly between the 7th and 3rd POD. In contrast, WPT and breakdown in the enterally fed rats decreased from the 3rd to the 7th POD (p<0.02). Protein breakdown on 7th POD had a positive correlation with urinary catecholamine excreation. The enterally fed rats had a higher FSR for skeletal muscle on both the 3rd and the 7th POD than the parenterally fed rats. The wound FSR on 3rd POD was also higher in the enterally fed rats than the parenterally fed rats. Protein synthesis in the small intestine was also increased in the enterally fed rats, which was reflected in the greater villus height in the small intestine. We conclude that postoperative enteral nutrition augments intestinal protein synthesis and the defense mechanism and thus causes lower stress than parenteral nutrition. Lower stress and increased protein synthesis in the intestine may decrease whole-body protein breakdown and enhance muscle protein synthesis in postoperative enteral nutrition. Therefore, postopeartive early enteral nutrition is recommended for improving protein metabolism in muscle, wounds, and the wholebody.

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The role of prostablandin E₂ (PGE₂) both on hepatic metastasis of colorectal carcinoma and on the local immunity at the primary site was investigated. Forty six patients with colorectal carcinoma were divided into two groups; 14 with liver metastasis (group A) and 32 without liver metastasis (group B). Samples were obtained from the draining vein, from the afferent artery, and from the peripheral vein. The level of PGE₂ was measured by RIA assay for each sample. The mean level of PGE₂ from the draining vein was higher than those from both the feeding artery and the peripheral vein. These differences were statistically significant. The V/A ratio of PGE₂ (PGE₂ level of the draining vein/PGE₂ level of the afferent artery) was also calculated. The V/A ratio of group A was significantly higher than that of group B. Histological (inflammatory cell infiltration), immunohistochemical (T cell subsets) and biochemical (inactivation of PGE₂) examinations were performed to determine the local immunity in about half of the patients. In patients with liver metastasis, inflammatory cell infiltration, IL-2 receptor positive cells infiltration and the inactivation of PGE₂ were decreased. We conclude that PGE₂ could play a role in suppressing local immunity and have adverse effect on liver metastasis.

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