title: Optimal alveolar oxygen concentration for cold storage of the lung.
abstract: BACKGROUND
  Ischemia of the lung is different from that of solid organs because the lung contains gas in the alveoli. However, the optimal gas composition in the alveoli during cold storage remains uncertain. We investigated the relationship between the alveolar oxygen concentration and reperfusion injury.
  
  
  METHODS
  The lungs inflated with 0% O2, 5% O2, room air, 50% O2, or 100% O2 were reperfused after 8 hR storage at 4 degrees C and pulmonary functions were measured for 120 min using an ex vivo rat lung model. The levels of high-energy phosphate and lipid peroxidation of the lung were analyzed after a PA flush, preservation, and reperfusion. Additionally, respiration of the mitochondria in the lungs was measured after preservation.
  
  
  RESULTS
  The pulmonary functions were significantly superior in the 5% O2 group than those in the 0% O2, 50% O2, and 100% O2 groups. Pulmonary edema developed in the 0% O2, 50% O2, and 100% O2 groups, but not in the 5% O2 group. After preservation, the energy level in the lungs decreased only in the 0% O2 group. Although lipid peroxidation of the lungs did not increase in any group after preservation, significant increases were observed in the room air, 50% O2 and 100% O2 groups after reperfusion. State 3 and 4 ratios of the mitochondrial respiration significantly decreased in the lungs of the room air, 50% O2 and 100% O2 groups.
  
  
  CONCLUSIONS
  Although the cold-preserved lungs require oxygen, hyperoxygenation induced mitochondrial dysfunction and increased lipid peroxidation and led to deleterious lung function after reperfusion. Therefore, hypoxic conditions that can maintain the energy level of the lung during cold storage would be optimal.
authors.affiliation: Department of Thoracic Surgery, Faculty of Medicine, Kyoto University, 54 Shogo-in Kawahara-cho, Sakyo-ku, Kyoto 606-8397, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Fukuse
authors.forename: T
authors.initials: T
authors.lastname: Hirata
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
authors.forename: T
authors.initials: T
authors.lastname: Shoji
authors.forename: T
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Q
authors.initials: Q
authors.lastname: Chen
authors.forename: T
authors.initials: T
authors.lastname: Matsukura
authors.forename: N
authors.initials: N
authors.lastname: Hanaoka
authors.forename: H
authors.initials: H
authors.lastname: Wada
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism*; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003080:Cold Temperature; D004734:Energy Metabolism; D015227:Lipid Peroxidation; D008168:Lung / Q000502:physiology; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D023421:Models, Animal; D009926:Organ Preservation / Q000379:methods*; D010100:Oxygen / Q000032:analysis* / Q000097:blood; D010101:Oxygen Consumption; D010477:Perfusion / Q000379:methods; D011175:Positive-Pressure Respiration; D011650:Pulmonary Alveoli / Q000502:physiology*; D051381:Rats; D011917:Rats, Inbred Lew; D015424:Reperfusion; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000227:Adenine Nucleotides; D017392:Thiobarbituric Acid Reactive Substances; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D010100:Oxygen