Enteral immunonutrition during sepsis prevents pulmonary dysfunction in a rat model.

BACKGROUND: Sepsis often results in severe pulmonary dysfunction. Via the thoracic duct, the lung is the first organ exposed to gut-derived inflammatory mediators released into mesenteric lymph during sepsis. AIM: To investigate whether an enteral immunonutrition during sepsis improves pulmonary function. METHODS: Mesenteric lymph was obtained from lymph fistula donor rats after intra peritoneal (i.p.) saline (control lymph) or lipopolysaccharide (sepsis lymph) injection. Sepsis lymph was also collected during enteral immunonutrition with omega-3 enriched, long-chain fatty acids (SMOF lipid). Control, sepsis, or sepsis-SMOF lymph was reinfused into the jugular vein of separate recipient rats. The lungs were then harvested, stained with hematoxylin-eosin, and analyzed for: (1) perpendicular parenchyma thickness of the alveolar wall; (2) myeloperoxidase-positive cells; and (3) terminal deoxynucleotidyl transferase Biotin-dUTP nick end labeling (TUNEL)-positive cells. RESULTS: Enteral immunonutrition during sepsis reduced the release of TNFalpha into mesenteric lymph by about 4.5-fold within the first 2 h. Infusion of sepsis lymph into recipient rats induced thickening of alveolar walls, inflammatory reaction, and apoptosis. Infusion of sepsis lymph obtained during enteral immunonutrition did not cause anatomical changes, induced only a mild inflammatory reaction, and prevented apoptosis in the lungs of recipient rats. CONCLUSIONS: Mediators in sepsis lymph induce pulmonary dysfunction such as an increased distance for oxygen transport, inflammatory reaction, and apoptosis. The lung may be protected by an enteral immunonutrition containing long-chain fatty acids.

Olive oil is more potent than fish oil to reduce septic pulmonary dysfunctions in rats.

BACKGROUND: Abdominal sepsis is frequently the cause of severe pulmonary dysfunction. Via the thoracic duct, the lung is the first organ exposed to gut-derived mediators released into the mesenteric lymph. AIM: The aim of this study is to investigate whether an enteral immunonutrition with long chain triglycerides prevents septic pulmonary dysfunctions. MATERIALS AND METHODS: Mesenteric lymph was obtained from lymph fistula donor rats during sepsis (lipopolysaccharides [LPS], 5 mg/kg i.p.) with or without enteral immunonutrition (1% of olive oil or 1% of fish oil). Sepsis lymph was then reinfused into the jugular vein of separate recipient rats. Thereafter, the lung tissue was analyzed for the distance of oxygen diffusion, inflammatory response, and cell apoptosis. RESULTS: Sepsis significantly increased TNFalpha release into the mesenteric lymph, whereas an enteral immunonutrition with olive oil significantly reduced the TNFalpha release into the mesenteric lymph by more than five-fold. Sepsis lymph induced a significant increase in alveolar wall thickness, inflammatory reaction, and apoptosis; whereas sepsis lymph collected during olive oil resorption prevented the thickening of the alveolar walls and induced only a mild inflammation, being more potent than fish oil to reduce septic pulmonary dysfunction. CONCLUSIONS: Mediators in the sepsis lymph induce pulmonary dysfunction. The lung may be protected by an enteral immunonutrition containing long chain triglycerides such as olive oil.