title: High-lipid enteral nutrition could partially mitigate inflammation but not lung injury in hemorrhagic shock rats.
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.
  
  
  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.
authors.affiliation: Department of Surgery, Buddhist Tzu Chi General Hospital, Taipei Branch, Taipei, Taiwan; School of Medicine, Tzu Chi University, Hualien, Taiwan; Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Bor-Gang
authors.initials: BG
authors.lastname: Wu
authors.forename: Tsui-Chin
authors.initials: TC
authors.lastname: Peng
authors.forename: Pei-Shan
authors.initials: PS
authors.lastname: Tsai
authors.forename: Tao-Yeuan
authors.initials: TY
authors.lastname: Wang
authors.forename: Mei-Jy
authors.initials: MJ
authors.lastname: Jeng
authors.forename: Chun-Jen
authors.initials: CJ
authors.lastname: Huang
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D054426:Chemokine CXCL2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D004750:Enteral Nutrition; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D015850:Interleukin-6 / Q000378:metabolism; D008055:Lipids / Q000008:administration & dosage / Q000627:therapeutic use*; D055370:Lung Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; D015850:Interleukin-6; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D015232:Dinoprostone
keywords: Acute lung injury; Hemorrhagic shock; High-lipid enteral nutrition; Inflammatory response; Oxidative stress; Rat; Resuscitation