title: Comparing the performance of rat lungs preserved for 6 or 12 hours after perfusion with low-potassium dextran or histidine-tryptophan-ketoglutarate.
abstract: BACKGROUND
  In lung transplantation, graft dysfunction is a frequent cause of mortality; the etiopathogenesis is related to ischemia-reperfusion injury. We sought to compare the lung performance of rats after reperfusion after presentation with 3 solutions at 2 ischemia times.
  
  
  METHODS
  We randomized 60 male Wistar rats to undergo anterograde perfusion via the pulmonary artery with low-potassium dextran (LPD), histidine-tryptophan ketoglutarate (HTK), or saline. After extraction, the heart-lung blocks were preserved in a solution at hypothermia for 6 or 12 hours before perfusion with homologous blood for 60 minutes using ex vivo system Isolated Perfused Rat or Guinea Pig Lung System (Harvard Apparatus). Respiratory mechanics, pulmonary weight, pulmonary artery pressure (PAP), and relative lung oxygenation capacity (ROC) measurements were obtained every 10 minutes.
  
  
  RESULTS
  Comparing tidal volume (TV), compliance, resistance, ROC, PAP, and pulmonary weight the LPD, HTK, and saline group did not differ at 6 and 12 hours. The TV was higher in the lungs with 6-hour ischemia in the LPD, HTK, and saline groups. Compliance was higher in the lungs with 6-hour ischemia in the LPD and saline groups. There were no differences in ROC values comparing lungs with 6- versus 12-hour ischemia in the LPD group. A significant difference was observed between lungs in the HTK and saline groups. Resistance was higher in the lungs with 12-hour ischemia among the LPD, HTK, and saline groups. There was a gradual weight increase in the lungs, particularly those undergoing 12-hour ischemia, despite the absence of a significant difference between groups.
  
  
  CONCLUSIONS
  Rat lungs perfused with LPD and HTK preservation solutions showed similar reperfusion performances in this ex-vivo perfusion model.
authors.affiliation: Department of Cardiopneumology, Medical School, University of São Paulo, Heart Institute, Hospital das Clínicas, São Paulo, Brazil.
authors.forename: E A
authors.initials: EA
authors.lastname: Simões
authors.forename: P M
authors.initials: PM
authors.lastname: Pêgo-Fernandes
authors.forename: P F G
authors.initials: PF
authors.lastname: Cardoso
authors.forename: R
authors.initials: R
authors.lastname: Pazetti
authors.forename: E
authors.initials: E
authors.lastname: Werebe
authors.forename: K A
authors.initials: KA
authors.lastname: de Oliveira Braga
authors.forename: A
authors.initials: A
authors.lastname: Menezes
authors.forename: N
authors.initials: N
authors.lastname: Nepomuceno
authors.forename: P R O
authors.initials: PR
authors.lastname: Soares
authors.forename: A T
authors.initials: AT
authors.lastname: Correia
authors.forename: F B
authors.initials: FB
authors.lastname: Jatene
mesh_terms: D000818:Animals; D003911:Dextrans; D005947:Glucose; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008168:Lung / Q000502:physiology*; D008297:Male; D008353:Mannitol; D010100:Oxygen / Q000378:metabolism; D010477:Perfusion; D011188:Potassium / Q000032:analysis*; D011189:Potassium Chloride; D011343:Procaine; D051381:Rats; D017208:Rats, Wistar
chemical_list: C039984:Bretschneider cardioplegic solution; D003911:Dextrans; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D005947:Glucose; D011188:Potassium; D010100:Oxygen