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The gastrointestinal tract, besides being the organ responsible for nutrient absorption, is also a metabolic and immunological system, functioning as an effective barrier against endotoxin and bacteria in the intestinal lumen.

Impairment of various functions of the liver and concomitantly increased levels of parameters of liver damage, a clinical entity termed liver failure, is commonly seen after partial hepatectomy. We investigated in a rat model whether damage of the remnant liver was due to local inflammatory responses, and related to endotoxin or interleukin-1 (IL-1). To address this question, the effects of partial hepatectomy on infiltration of immunocompetent cells and expression of major histocompatibility complex (MHC) class II antigen of macrophages in the remnant liver was studied using immunohistochemical techniques. Specific intervention with recombinant N-terminal bactericidal/permeability-increasing protein (rBPI23) to neutralize endotoxin and with IL-1 receptor antagonist (IL-1ra) to block IL-1 activity was used to examine the respective roles of endotoxin and IL-1. After partial hepatectomy, we found an influx of neutrophils, an increased expression of MHC class II antigens, and morphologic changes of Kupffer cells consistent with activation. These inflammatory events coincided with increased serum levels of markers of liver damage (aspartate aminotransferase, alanine aminotransferase, ammonia). Both neutralization of endotoxin and blocking of IL-1 activity reduced hepatic inflammation and reduced serum levels of aminotransferases and ammonia. In addition, liver cell proliferation as assessed by staining for proliferating cell nuclear antigen (PCNA) expression was significantly enhanced when either endotoxin or IL-1 effects were blocked. Thus, our results suggest that local hepatic inflammatory responses inhibit liver cell proliferation and promote liver failure, presumably by affecting the functional capacity of the remnant liver.

The findings indicate that enteral Gln supplementation caused significantly increased arterial plasma levels of Arg as a result of increased renal Arg production from circulating citrulline. Considering the multiple important biologic properties of Arg, the reported beneficial effects of Gln in catabolic states might be explained in part by increased renal Arg production.

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The hemodynamic consequences of glutamine (Gln)-enriched nutrition have not been investigated. This study investigates the effects of a Gln-enriched enteral diet on organ blood flows and systemic hemodynamics. Male Fischer 344 rats (n = 24) were randomized to a group that received a 12.5% (wt/wt) Gln-enriched enteral diet or an isonitrogenous isocaloric control diet for 14 days. Blood flow measurements were performed at day 16 using 46Sc-labeled microspheres. In the Gln-enriched group, higher organ blood flows were measured in the stomach (51%), the pancreas (35%), small intestine (32%), and colon (55%), compared with controls. No differences were found in systemic hemodynamic parameters between the control and Gln-supplemented groups. A possible role for nitric oxide in this splanchnic vasodilation was investigated. Daily urinary nitrate excretion was measured during the study but showed no significant differences between the control and Gln-fed animals. No differences were found in plasma levels of the vasodilating hormone glucagon between the groups. These results show that a Gln-enriched enteral diet increased splanchnic blood flow, which was not mediated by pancreatic glucagon or increased nitric oxide production as determined by urinary nitrate excretion.