title: When is injury potentially reversible in a lung ischemia-reperfusion model?
abstract: OBJECTIVE
  To verify the impact of ischemic time on lung cell viability in an experimental model of lung ischemia-reperfusion (IR) injury and its repercussion on lung performance after reperfusion.
  
  
  METHODS
  Twenty-four animals were subjected to selective clamping of the left pulmonary artery and divided into four groups (n = 6) according to ischemic time: 15 (IR15), 30 (IR30), 45 (IR45), and 60 min (IR60). All animals were observed for 120 min after reperfusion. The hemodynamics, arterial blood gases measurements, and histologic changes were analyzed. Immunofluorescence assays for caspase 3 and annexin V were performed. Lipid peroxidation was assessed by thiobarbituric acid-reactive substances, and caspase 3 activity was assessed by colorimetric extract.
  
  
  RESULTS
  The partial pressure of arterial oxygen significantly decreased at the end of the observation period in the IR30, IR45, and IR60 groups (P < 0.05). The final mean arterial pressure significantly decreased in the IR60 group (P < 0.05). We observed a significant increase in caspase 3 activity and caspase 3-positive cells by immunofluorescence in the IR45 group compared with the other groups (P < 0.05). Additionally, there was an increase in necrotic cells assessed by annexin V in the IR60 group. The histologic score did not show differences among the different groups.
  
  
  CONCLUSIONS
  The degree of cell damage had a negative impact on lung performance. Sixty minutes of lung ischemia and posterior reperfusion resulted in an increased number of necrotic cells, suggesting that these cells may not be able to reverse the effects of the IR injury because of the lack of viable cells.
authors.affiliation: Physiotherapy Department, Methodist University, IPA, Porto Alegre, Brazil.
authors.forename: Luiz Alberto
authors.initials: LA
authors.lastname: Forgiarini
authors.forename: Gustavo
authors.initials: G
authors.lastname: Grün
authors.forename: Nélson Alexandre
authors.initials: NA
authors.lastname: Kretzmann
authors.forename: Gustavo Alfredo Ochs
authors.initials: GA
authors.lastname: de Muñoz
authors.forename: Antonino
authors.initials: A
authors.lastname: de Almeida
authors.forename: Luiz Felipe
authors.initials: LF
authors.lastname: Forgiarini
authors.forename: Cristiano Feijó
authors.initials: CF
authors.lastname: Andrade
mesh_terms: D000818:Animals; D017304:Annexin A5 / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology; D001784:Blood Gas Analysis; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D008168:Lung / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D008171:Lung Diseases / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D008297:Male; D023421:Models, Animal; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D017304:Annexin A5; D017392:Thiobarbituric Acid Reactive Substances; D053148:Caspase 3