title: Impact of the cardiac arrest mode on cardiac death donor lungs.
abstract: BACKGROUND
  Donation after cardiac death (DCD) organs could alleviate the shortage of donor lungs. This study aimed to assess the influence on lung injuries of the way in which cardiac arrest was induced and to investigate the mechanisms leading to any differences.
  
  
  METHODS
  Male rats were allocated into three groups as follows: sham (no warm ischemia), ventricular fibrillation (VF), and asphyxia group. Cardiac arrest was induced by either VF by way of a fibrillator or asphyxia caused by withdrawal of ventilation, which reflected uncontrolled and controlled DCD situations, respectively. The impact on lung flushing after 60 min of warm ischemia time was evaluated (n = 5, in each group). The physiological functions of the lungs in an isolated lung perfusion circuit were also evaluated with warm ischemia time prolonged to 150 min (n = 8, in each group). Messenger RNA expression levels of surfactant proteins (SPs) and inflammatory cytokines, pathologic findings, and high-energy phosphates of the lung tissues were investigated.
  
  
  RESULTS
  In the asphyxia group, flushing and physiological functions in the isolated lung perfusion circuit were the most severely affected. Reverse transcription-polymerase chain reaction and pathologic findings revealed depletion of surfactant protein (SP)-C in lung tissues of the asphyxia group after reperfusion. The VF group was characteristic with elevated pulmonary vascular resistance.
  
  
  CONCLUSIONS
  Lung injuries were mainly attributed to alveolar wall damage and depletion of SP in the asphyxia group, and perivascular area prominent edema in the VF group. DCD donor lungs were affected differently by the way in which cardiac arrest was induced.
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yamada
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Fengshi
authors.initials: F
authors.lastname: Chen
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Jin
authors.initials: J
authors.lastname: Sakamoto
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Nakajima
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Ohsumi
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Bando
authors.affiliation: Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. Electronic address: hdate@kuhp.kyoto-u.ac.jp.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Date
mesh_terms: D000818:Animals; D003643:Death; D006323:Heart Arrest; D008168:Lung / Q000473:pathology; D016040:Lung Transplantation; D008297:Male; D010455:Peptides / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew; D015424:Reperfusion; D014019:Tissue Donors
chemical_list: D010455:Peptides; C077063:Sftpc protein, rat
keywords: Donation after cardiac death; Donor; Ischemia–reperfusion injury; Lung transplantation