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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 590987, 14 pages
Review Article

Oxidative Stress and Lung Ischemia-Reperfusion Injury

1Thoracic Surgery Department, Laboratory of Airways and Lung, Hospital of Clínicas of Porto Alegre, Ramiro Barcelos 2.350, 90035-903 Porto Alegre, RS, Brazil
2Federal University of Rio Grande of Sul (FRGS), Rua Ramiro Barcelos 2400, 2° andar Bairro Santana, 90035-003 Porto Alegre, RS, Brazil

Received 19 October 2014; Revised 19 January 2015; Accepted 20 January 2015

Academic Editor: Zhengyuan Xia

Copyright © 2015 Renata Salatti Ferrari and Cristiano Feijó Andrade. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.