title: Reperfusion lung injury after cold preservation correlates with decreased levels of intrapulmonary high-energy phosphates.
abstract: BACKGROUND
  To evaluate the role of energy state in primary graft dysfunction, which is crucial in lung transplantation, we investigated the relationship between intrapulmonary high-energy phosphate compounds and reperfusion lung injury after cold preservation.
  
  
  METHODS
  Using an isolated rat lung perfusion model with fresh rat blood as perfusate, rat lungs were exposed to various cold preservation periods (0, 6, 9, and 12 hr) and reperfused.
  
  
  RESULTS
  We found that extending the preservation period exacerbated the pulmonary hemodynamics after reperfusion. The levels of intrapulmonary high-energy phosphate compounds did not change during cold preservation, but these levels after reperfusion decreased as the preservation period was prolonged. The pulmonary hemodynamics after reperfusion were inversely correlated with the intrapulmonary high-energy phosphate compound levels after reperfusion. Total adenine nucleotide and ATP were sensitive indicators of reperfusion lung injury after cold preservation. Energy charge was not a sensitive indicator. The decreased levels of intrapulmonary high-energy phosphate compounds after reperfusion following cold preservation period were partially caused by their decreased production.
  
  
  CONCLUSIONS
  These results demonstrated that reperfusion lung injury after cold preservation was closely correlated with decreased levels of intrapulmonary high-energy phosphate compounds after reperfusion, although the levels of the intrapulmonary high-energy phosphate compounds did not change during cold preservation of up to 12 hr.
authors.affiliation: Department of Thoracic Surgery, Faculty of Medicine, Kyoto University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Hirata
authors.forename: T
authors.initials: T
authors.lastname: Fukuse
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Kawashima
authors.forename: S
authors.initials: S
authors.lastname: Hitomi
authors.forename: H
authors.initials: H
authors.lastname: Wada
mesh_terms: D000227:Adenine Nucleotides / Q000032:analysis*; D000244:Adenosine Diphosphate / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D003080:Cold Temperature; D004730:Endothelium, Vascular / Q000648:ultrastructure; D006439:Hemodynamics; D008168:Lung / Q000378:metabolism*; D008297:Male; D009926:Organ Preservation; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000378:metabolism*; D013997:Time Factors
chemical_list: D000227:Adenine Nucleotides; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate