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Review
. 2017 Mar;5(6):131.
doi: 10.21037/atm.2017.03.32.

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

Jan F Gielis  1   2 , Paul A J Beckers  1 , Jacco J Briedé  3 , Paul Cos  2 , Paul E Van Schil  1
Affiliations
Review

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

Jan F Gielis et al. Ann Transl Med. 2017 Mar.

Abstract

Oxidative and nitrosative stress are an umbrella term for pathophysiological processes that involve free radical generation during inflammation. In this review, the involvement of reactive oxygen and nitrogen species is evaluated during lung ischemia-reperfusion injury (LIRI) from a surgical point of view. The main biochemical and cellular mechanisms behind free radical generation are discussed, together with surgical procedures that may cause reperfusion injury. Finally, different therapeutic strategies are further explored. A literature search was performed, searching for "lung ischemia reperfusion injury", "reperfusion injury", "large animal model" and different search terms for each section: "surgery", "treatment", "cellular mechanism", or "enzyme". Although reperfusion injury is not an uncommon entity and there is a lot of evidence concerning myocardial ischemia-reperfusion injury, in the lung this phenomenon is less extensively described and studies in large animals are not easy to come by. With increasing number of patients on waiting lists for lung transplant, awareness for this entity should all but rise.

Keywords: Ischemia reperfusion injury; nitrosative stress; oxidative stress; reactive nitrogen species (RNS); reactive oxygen species (ROS).

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation in the endothelial cells by combined effects of eNOS uncoupling, xanthine dehydrogenase conversion and NOX induction.
Figure 2
Figure 2
Dashed lines depict the pathways leading to mitochondrial uncoupling, which take place when increased amounts of reactive oxygen species (ROS) are produced, causing the assembly of the mitochondrial permeability transition pore (mPTP) complex and subsequent cell death. Full lines express normal physiological pathways.
Figure 3
Figure 3
Biochemical reactions catalyzed by iron leading to increased oxidative stress formation and different enzyme systems responsible for neutralization of free radicals.
See this image and copyright information in PMC

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