Oxidative Stress and Lung Ischemia-Reperfusion Injury

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...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2015-01, Vol.2015 (2015), p.1-14
Main Authors: Salatti Ferrari, Renata, Andrade, Cristiano Feijó
Format: Article
Language:English
Subjects:
Adenosine
Analysis
Animals
Antioxidants - metabolism
Apoptosis
Calcium Channels - metabolism
Cytokines
Cytotoxicity
Dehydrogenases
Edema
Endothelium
Enzymes
Free radicals
Heart attacks
Humans
Hypoxia
Inflammation
Inflammation Mediators - metabolism
Ischemia
Lung - metabolism
Lung diseases
Metabolites
Oxidative Stress
Permeability
Phosphorylation
Poisoning
Reactive Oxygen Species - metabolism
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Review
Rodents
Sodium Channels - metabolism
Studies
Thoracic surgery
Transplantation of organs, tissues, etc
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Summary: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.
ISSN:1942-0900
1942-0994
DOI:10.1155/2015/590987