title: The effect of LPS on cytokine synthesis and lung neutrophil influx after hepatic ischemia/reperfusion injury in the rat.
abstract: OBJECTIVE
  To determine if cytokine responses and lung injury induced by intravenous (i.v.) lipopolysaccharide (LPS) at 4 hr were enhanced in rats that had been previously subjected to 30 min of total liver ischemia (Pringle's maneuver) followed by 24 hr or 3 days of reperfusion.
  
  
  BACKGROUND
  Many patients with liver trauma require occlusion of hepatic blood flow to control hemorrhage and facilitate repair. A significant number of these patients subsequently develop the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction (MOD) characterized by the release of cytokines and tissue neutrophil influx. Macrophages, including Kupffer cells, may be activated by ischemic injury and dysregulation of their response to LPS may contribute to the development of SIRS and acute respiratory distress syndrome.
  
  
  METHODS
  Adult male Sprague-Dawley rats were randomly divided into six groups: three groups received total hepatic ischemia for 30 min and three groups had a sham procedure. Twenty-four hours or 3 days after hepatic ischemia/reperfusion injury, rats were treated with LPS (5 mg/kg) or saline and monitored for 4 hr. We collected serum, bronchoalveolar lavage (BAL) fluid, and lung tissue.
  
  
  RESULTS
  Serum and BAL cytokine concentrations were significantly increased by i.v. LPS; however, hepatic ischemia/reperfusion injury 24 hr or 3 days before iv LPS ameliorated this cytokine response. The LPS-induced pulmonary neutrophil influx and histopathological changes were similar in sham and hepatic ischemia/reperfusion-injured groups.
  
  
  CONCLUSIONS
  Hepatic ischemia/reperfusion injury significantly attenuated the serum and BAL cytokine concentrations, but did not change pulmonary neutrophil influx or histopathological alterations in response to i.v. LPS.
authors.affiliation: Department of Anesthesiology, Graduate School of Medicine, University of Tenneesee Medical Center, Knoxville 37920, USA.
authors.forename: J B
authors.initials: JB
authors.lastname: Carrick
authors.forename: O
authors.initials: O
authors.lastname: Martins
authors.forename: C C
authors.initials: CC
authors.lastname: Snider
authors.forename: N D
authors.initials: ND
authors.lastname: Means
authors.forename: B L
authors.initials: BL
authors.lastname: Enderson
authors.forename: S B
authors.initials: SB
authors.lastname: Frame
authors.forename: S A
authors.initials: SA
authors.lastname: Morris
authors.forename: M D
authors.initials: MD
authors.lastname: Karlstad
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D054426:Chemokine CXCL2; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D016207:Cytokines / Q000097:blood*; D007275:Injections, Intravenous; D015850:Interleukin-6 / Q000032:analysis / Q000097:blood; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008099:Liver / Q000098:blood supply*; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000473:pathology*; D008297:Male; D015846:Monokines / Q000032:analysis / Q000097:blood; D009504:Neutrophils / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D054426:Chemokine CXCL2; D016207:Cytokines; D015850:Interleukin-6; D008070:Lipopolysaccharides; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase