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Eur J Cardiothorac Surg 2006;29:294-298
© 2006 Elsevier Science NL

Effect of lung ischemia–reperfusion on oxidative stress parameters of remote tissues

^a Department of Thoracic Surgery, Afyon Kocatepe University, School of Medicine, 03200 Afyon, Turkey
^b Department of Anaesthesia, Kocatepe University, School of Medicine, Afyon, Turkey
^c Department of Biochemistry, Kocatepe University, School of Medicine, Afyon, Turkey

Received 24 May 2005; received in revised form 6 December 2005; accepted 6 December 2005.

^_* Corresponding author. Tel.: +90 533 6471729; fax: +90 272 2172029. (Email: hesme{at}aku.edu.tr).

Objective: Ischemia–reperfusion injury induces a systemic inflammatory response and production of reactive oxygen species, which potentially can be more detrimental than its local effects. Although the lung injury that is formed by the effects of ischemia–reperfusion injury on remote organs has been previously studied, no previous study that investigated the effects of pulmonary ischemia–reperfusion injury on remote organs has been considered. We hypothesized that the lung ischemia–reperfusion injury may cause the spread of inflammation to remote organs such as liver and heart. Methods: Thirty New Zealand white rabbits were subjected to either sham operation or lung ischemia–reperfusion injury in various periods of time (60 min ischemia–60 min reperfusion and 120 min ischemia–60 min reperfusion, respectively). Pulmonary, myocardial and hepatic myeloperoxidase, protein sulfhydryl, thiobarbituric acid-reactive substances, and protein carbonyl levels were evaluated to show pulmonary, hepatic, and myocardial responses to lung ischemia–reperfusion injury. Results: Reperfusion after 60 min of lung ischemia led to increased myeloperoxidase and protein carbonyl levels and decreased protein sulfhydryl groups in pulmonary tissue, increased myeloperoxidase and decreased protein sulfhydryl groups in hepatic tissue, and increased myeloperoxidase, thiobarbituric acid-reactive substances and protein carbonyl levels in myocardial tissue. Reperfusion after 120 min of lung ischemia led to increased thiobarbituric acid-reactive substance levels in pulmonary tissue, increased protein carbonyl and thiobarbituric acid-reactive substance levels in hepatic tissue, and decreased protein sulfhydryl groups in myocardial tissue. Conclusions: The data of the present study suggests that pulmonary ischemia–reperfusion induces liver and heart injury characterized by activated neutrophil sequestration and release of significant amounts of reactive oxygen species. The remote organ injury has to be kept in mind when performing a lung intervention or surgery and care should be taken to protect other organs remote from ischemia–reperfusion site.

Key Words: Remote injury • Lung • Liver • Heart

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