title: Experimental acute pancreatitis induces mitochondrial dysfunction in rat pancreas, kidney and lungs but not in liver.
abstract: OBJECTIVE
  Excessive systemic inflammatory response syndrome during severe acute pancreatitis (AP) leads to multiple organ dysfunction syndrome, which is the main cause of death and may be associated with primary mitochondrial disturbances. The aim of our study was to evaluate the role of mitochondria during experimental AP in pancreas and vital organs like kidney, lungs and liver within the first 48 h.
  
  
  METHODS
  AP was induced in 39 male Wistar rats by intraductal application of sodium taurocholate (5%, 1.75 ml/kg). Animals were divided into groups reflecting the time from induction of the AP till collection of tissues (control and 1, 3, 6, 12, 24, 48 h). Mitochondria were isolated by differential centrifugation and mitochondrial respiration rates were measured oxygraphically.
  
  
  RESULTS
  (1) Mitochondria in pancreas are affected within the first 6 h after onset of AP, (2) kidney mitochondria are affected 24 h after onset of AP, (3) lungs mitochondria are affected within 48 h after onset of AP whereas (4) liver mitochondria remain well preserved within the first 48 h. Severe AP-induced decrease in the oxidative phosphorylation of pancreas, kidney and lungs mitochondria was more pronounced with Complex I-linked (glutamate/malate) than with Complex II-linked (succinate) substrates and was associated with inhibition of Complex I.
  
  
  CONCLUSIONS
  Our data show that the disturbances of mitochondrial energy metabolism in pancreas, kidney and lungs may play an important role in the development and progression of AP as a systemic disease.
authors.affiliation: Institute of Neurosciences, Medical Academy, Lithuanian University of Health Sciences, Eiveniu Str. 4, Kaunas, Lithuania. sonatai@centras.lt
authors.forename: Sonata
authors.initials: S
authors.lastname: Trumbeckaite
authors.forename: Irma
authors.initials: I
authors.lastname: Kuliaviene
authors.forename: Olegas
authors.initials: O
authors.lastname: Deduchovas
authors.forename: Marius
authors.initials: M
authors.lastname: Kincius
authors.forename: Rasa
authors.initials: R
authors.lastname: Baniene
authors.forename: Simona
authors.initials: S
authors.lastname: Virketyte
authors.forename: Dovidas
authors.initials: D
authors.lastname: Bukauskas
authors.forename: Eugene
authors.initials: E
authors.lastname: Jansen
authors.forename: Limas
authors.initials: L
authors.lastname: Kupčinskas
authors.forename: Vilmante
authors.initials: V
authors.lastname: Borutaite
authors.forename: Antanas
authors.initials: A
authors.lastname: Gulbinas
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004734:Energy Metabolism; D007668:Kidney / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D028361:Mitochondrial Diseases / Q000209:etiology*; D009102:Multiple Organ Failure / Q000209:etiology; D010179:Pancreas / Q000503:physiopathology*; D010195:Pancreatitis / Q000139:chemically induced / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid
chemical_list: D013656:Taurocholic Acid