Limits...
Oxidative Stress and Lung Ischemia-Reperfusion Injury.

Ferrari RS, Andrade CF - Oxid Med Cell Longev (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

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

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Activation of the immune response and trafficking of inflammatory cells in the diseased organ during reperfusion.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4487720&req=5

fig2: Activation of the immune response and trafficking of inflammatory cells in the diseased organ during reperfusion.

Mentions: For example, when TLRs recognize specific molecules, they trigger the activation of signaling pathways, including the NF-κB activation of protein kinase (MAPK) pathways and type I interferon, which results in the induction of proinflammatory cytokines and chemokines. These receptors can also be activated by endogenous molecules in the absence of microbial compounds, particularly within the context of cell damage or death, as occurs during IR [78] (Figure 2).


Oxidative Stress and Lung Ischemia-Reperfusion Injury.

Ferrari RS, Andrade CF - Oxid Med Cell Longev (2015)

Activation of the immune response and trafficking of inflammatory cells in the diseased organ during reperfusion.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487720&req=5

fig2: Activation of the immune response and trafficking of inflammatory cells in the diseased organ during reperfusion.
Mentions: For example, when TLRs recognize specific molecules, they trigger the activation of signaling pathways, including the NF-κB activation of protein kinase (MAPK) pathways and type I interferon, which results in the induction of proinflammatory cytokines and chemokines. These receptors can also be activated by endogenous molecules in the absence of microbial compounds, particularly within the context of cell damage or death, as occurs during IR [78] (Figure 2).

Bottom Line: 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.

View Article: PubMed Central - PubMed

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

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus