High-lipid enteral nutrition could partially mitigate inflammation but not lung injury in hemorrhagic shock rats

J Surg Res. 2013 Oct;184(2):997-1005. doi: 10.1016/j.jss.2013.03.085. Epub 2013 Apr 17.

Abstract

Background: Loss of gut barrier function is crucial in mediating lung injury induced by hemorrhagic shock/resuscitation (HS). High-lipid enteral nutrition (HL) can preserve gut barrier function. We hypothesized that HL could also mitigate HS-induced lung injury.

Materials and methods: Forty-eight adult male rats were randomly assigned to one of four experimental groups: HS; HS-HL; Sham; Sham-HL. HS was induced by blood drawing and mean blood pressure was maintained at 40-45 mmHg for 120 min followed by resuscitation with re-infusion of exsanguinated blood/saline mixtures. HL gavage was performed at 45 min before blood drawing and at the end of resuscitation.

Results: Intestinal permeability of the HS group was significantly higher than that of the Sham group (P < 0.001). Pulmonary concentrations of malondialdehyde (lipid peroxidation) and inflammatory molecules, including prostaglandin E2, tumor necrosis factor-α, interleukin-6, and macrophage inflammatory protein-2, of the HS group were significantly higher than those of the Sham group. Histologic analyses, including histopathology, wet/dry weight ratio, and neutrophil infiltration revealed moderate lung injury in the HS group. In contrast, intestinal permeability (P < 0.001) and pulmonary concentrations of tumor necrosis factor-α and macrophage inflammatory protein-2 (P = 0.021 and 0.01) of the HS-HL group were significantly lower than those of the HS group. However, pulmonary concentrations of malondialdehyde, prostaglandin E2, and interleukin-6 of the HS-HL and HS groups were comparable. Moreover, histologic analyses also revealed moderate lung injury in the HS-HL group.

Conclusions: High-lipid enteral nutrition significantly mitigated gut barrier loss and partially mitigated lung inflammation but not oxidation and lung injury in hemorrhagic shock/resuscitation rats.

Keywords: Acute lung injury; Hemorrhagic shock; High-lipid enteral nutrition; Inflammatory response; Oxidative stress; Rat; Resuscitation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Pressure / physiology
  • Chemokine CXCL2 / metabolism
  • Dinoprostone / metabolism
  • Disease Models, Animal
  • Enteral Nutrition*
  • Inflammation / etiology
  • Inflammation / metabolism
  • Inflammation / prevention & control*
  • Interleukin-6 / metabolism
  • Lipids / administration & dosage
  • Lipids / therapeutic use*
  • Lung Injury / etiology
  • Lung Injury / metabolism
  • Lung Injury / prevention & control*
  • Male
  • Malondialdehyde / metabolism
  • Oxidative Stress / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Shock, Hemorrhagic / complications*
  • Shock, Hemorrhagic / metabolism*
  • Shock, Hemorrhagic / physiopathology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CXCL2
  • Interleukin-6
  • Lipids
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Dinoprostone