title: Hepatic effects of an open lung strategy and cardiac output restoration in an experimental lung injury.
abstract: BACKGROUND
  Ventilation with high positive end-expiratory pressure (PEEP) can lead to liver dysfunction. We hypothesized that an open lung concept (OLC) using high PEEP impairs liver function and integrity dependent on the stabilization of cardiac output.
  
  
  METHODS
  Juvenile female Pietrain pigs instrumented with flow probes around the common hepatic artery and portal vein, pulmonary and hepatic vein catheters underwent a lavage-induced lung injury. Ventilation was continued with a conventional approach (CON) using pre-defined combinations of PEEP and inspiratory oxygen fraction or with an OLC using PEEP set above the lower inflection point of the lung. Volume replacement with colloids was guided to maintain cardiac output in the CON(V+) and OLC(V+) groups or acceptable blood pressure and heart rate in the OLC(V-) group. Indocyanine green plasma disappearance rate (ICG-PDR), blood gases, liver-specific serum enzymes, bilirubin, hyaluronic acid and lactate were tested. Finally, liver tissue was examined for neutrophil accumulation, TUNEL staining, caspase-3 activity and heat shock protein 70 mRNA expression.
  
  
  RESULTS
  Hepatic venous oxygen saturation was reduced to 18 + or - 16% in the OLC(V-) group, while portal venous blood flow decreased by 45%. ICG-PDR was not reduced and serum enzymes, bilirubin and lactate were not elevated. Liver cell apoptosis was negligible. Liver sinusoids in the OLC(V+) and OLC(V-) groups showed about two- and fourfold more granulocytes than the CON(V+) group. Heat shock protein 70 tended to be higher in the OLC(V-) group.
  
  
  CONCLUSIONS
  Open lung ventilation elicited neutrophil infiltration, but no liver dysfunction even without the stabilization of cardiac output.
authors.affiliation: Department of Anaesthesia and Critical Care, University of Würzburg, Oberdürrbacherstrasse 6, 97080 Würzburg, Germany. kredel_m@klinik.uni-wuerzburg.de
authors.forename: M
authors.initials: M
authors.lastname: Kredel
authors.forename: R M
authors.initials: RM
authors.lastname: Muellenbach
authors.forename: A
authors.initials: A
authors.lastname: Hornung
authors.forename: R
authors.initials: R
authors.lastname: Schmidt
authors.forename: J
authors.initials: J
authors.lastname: Laqua
authors.forename: J
authors.initials: J
authors.lastname: Brederlau
authors.forename: N
authors.initials: N
authors.lastname: Roewer
authors.forename: C
authors.initials: C
authors.lastname: Wunder
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology*; D053148:Caspase 3 / Q000032:analysis; D004195:Disease Models, Animal; D005260:Female; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006820:Hyaluronic Acid / Q000032:analysis; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008111:Liver Function Tests; D055370:Lung Injury / Q000150:complications / Q000503:physiopathology*; D020556:Neutrophil Infiltration / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011175:Positive-Pressure Respiration / Q000009:adverse effects*; D011897:Random Allocation; D012119:Respiration; D013552:Swine
chemical_list: D018840:HSP70 Heat-Shock Proteins; D006820:Hyaluronic Acid; D053148:Caspase 3; D010100:Oxygen