• Tetsu Yamada, Fengshi Chen, Jin Sakamoto, Daisuke Nakajima, Akihiro Ohsumi, Toru Bando, and Hiroshi Date.
• Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
• J. Surg. Res. 2015 May 15; 195 (2): 596-603.

BackgroundDonation 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.Materials And MethodsMale 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.ResultsIn 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.ConclusionsLung 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.Copyright © 2015 Elsevier Inc. All rights reserved.

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