title: Hepatic effects of lung-protective pressure-controlled ventilation and a combination of high-frequency oscillatory ventilation and extracorporeal lung assist in experimental lung injury.
abstract: BACKGROUND
  Ventilation with high positive end-expiratory pressure (PEEP) can lead to hepatic dysfunction. The aim of this study was to investigate the hepatic effects of strategies using high airway pressures either in pressure-controlled ventilation (PCV) or in high-frequency oscillatory ventilation (HFOV) combined with an arteriovenous extracorporeal lung assist (ECLA).
  
  
  METHODS
  Pietrain pigs underwent induction of lung injury by saline lavage. Ventilation was continued for 24 hours either as PCV with tidal volumes of 6 ml/kg and PEEP 3 cmH2O above the lower inflection point of the pressure-volume curve or as HFOV (≥ 12 Hz) with a mean tracheal airway pressure 3 cmH2O above the lower inflection point combined with arteriovenous ECLA (HFOV+ECLA). Fluids and norepinephrine stabilized the circulation. The indocyanine green plasma disappearance rate, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, alkaline phosphatase, glutamate dehydrogenase, lactate dehydrogenase and creatine kinase were determined repeatedly. Finally, liver neutrophils were counted and liver cell apoptosis was assessed by terminal deoxynucleotidyl transferase nick end labeling (TUNEL).
  
  
  RESULTS
  Aspartate aminotransferase increased in the PCV group about three-fold and in the HFOV+ECLA group five-fold (p<0.001). Correspondingly, creatine kinase increased about two-fold and four-fold, respectively (p<0.001). Lactate dehydrogenase was increased in the HFOV+ECLA group (p<0.028). The number of neutrophils infiltrating the liver tissue and the apoptotic index were low.
  
  
  CONCLUSIONS
  High airway pressure PCV and HFOV with ECLA in the treatment of lavage-induced lung injury in pigs did not cause liver dysfunction or damage. The detected elevation of enzymes might be of extrahepatic origin.
authors.affiliation: Department of Anaesthesia and Critical Care, University of Würzburg, Würzburg, Germany.
authors.forename: Markus
authors.initials: M
authors.lastname: Kredel
authors.forename: Ralf M
authors.initials: RM
authors.lastname: Muellenbach
authors.forename: Amélie
authors.initials: A
authors.lastname: Johannes
authors.forename: Joerg
authors.initials: J
authors.lastname: Brederlau
authors.forename: Norbert
authors.initials: N
authors.lastname: Roewer
authors.forename: Christian
authors.initials: C
authors.lastname: Wunder
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001219:Aspartate Aminotransferases / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D006612:High-Frequency Ventilation / Q000009:adverse effects* / Q000379:methods*; D020287:In Situ Nick-End Labeling; D059725:Interactive Ventilatory Support / Q000379:methods; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000473:pathology*; D055370:Lung Injury / Q000628:therapy*; D009504:Neutrophils; D011175:Positive-Pressure Respiration / Q000009:adverse effects* / Q000379:methods*; D034421:Sus scrofa
chemical_list: D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase