Lung ischemia–reperfusion injury: implications of oxidative stress and platelet–arteriolar wall interactions

Ovechkin, Alexander V.; Lominadze, David; Sedoris, Kara C.; Robinson, Tonya; Tyagi, Suresh C.; Roberts, Andrew M.

doi:10.1080/13813450601118976

Cited by 101 publications

(87 citation statements)

References 190 publications

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“…NO is a powerful anti-inflammatory agent, decreasing leukocyte recruitment (83) and the subsequent release of inflammatory cytokines. Although this is normally a beneficial effect, in high concentrations NO may also react with ROS to form peroxynitrite and other reactive nitrogen species (73,160). Of these NOS subtypes, the activities of eNOS and iNOS have been shown to be anti-inflammatory in several models (44,83), although the overinduction of iNOS is implicated in the formation of reactive nitrogen species (160).…”

Section: Mechanisms Of Lung Injury During Irmentioning

confidence: 99%

Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process

Hengst

Gielis

Lin

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

308

280

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Lung ischemia-reperfusion injury remains one of the major complications after cardiac bypass surgery and lung transplantation. Due to its dual blood supply system and the availability of oxygen from alveolar ventilation, the pathogenetic mechanisms of ischemia-reperfusion injury in the lungs are more complicated than in other organs, where loss of blood flow automatically leads to hypoxia. In this review, an extensive overview is given of the molecular and cellular mechanisms that are involved in the pathogenesis of lung ischemia-reperfusion injury and the possible therapeutic strategies to reduce or prevent it. In addition, the roles of neutrophils, alveolar macrophages, cytokines, and chemokines, as well as the alterations in the cell-death related pathways, are described in detail. pulmonary; lung transplantation; ventilated ischemia IN THE PAST, THE LUNG WAS thought to be relatively resistant to ischemia because of its dual circulation and the availability of oxygen from alveolar ventilation. However, the depletion of lung oxygenation by stopping the ventilation leads to the same degree of lung impairment as a decrease in mechanotransduction by loss of blood flow, as determined by increases in vascular pressure and permeability (11), indicating that any deficiency from oxygenation or mechanotransduction can have significant repercussions (149).Reperfusion of the ischemic lung is a double-edged sword. Reestablishing the perfusion of the ischemic lung is absolutely required to maintain the viability of the lung, but reperfusion itself can trigger a complex cascade of events, the so-called pulmonary ischemia-reperfusion injury (LIRI) (48), characterized by increased microvascular permeability (Pvasc), increased pulmonary vascular resistance (PVR), pulmonary edema, impaired oxygenation, and pulmonary hypertension. Ischemia of the lung, without loss of ventilation, results in a complex pathophysiological situation and, therefore, is not comparable with ischemia in other organs. During ventilated ischemia, for example, the adenosine triphosphate (ATP) levels remain normal while reactive oxygen species (ROS) are formed (70), illustrating aspects of complexity of the pathophysiology of ventilated and anoxic lung ischemia. Therefore, a distinction should be made between ventilated ischemia, meaning a loss of blood flow, and anoxia/reoxygenation, indicating the loss of oxygenation and/or perfusion. In this review, the terms anoxia/reoxygenation and ventilated ischemia will be used, if the specific model is known and/or the mechanism is suggested to be model specific. Ischemia alone will be used, if it applies for both mechanisms, if the specific model is not known, or the research involves other organs.Complete and prolonged lung anoxia for up to several hours is unavoidable during lung transplantation, with dire consequences. Reperfusion of the transplanted lung can lead to nonspecific alveolar damage, pulmonary edema, and hypoxemia within 72 h after lung transplantation. Even with the advancements in lung preservati...

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Section: Mechanisms Of Lung Injury During Irmentioning

confidence: 99%

Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process

Hengst

Gielis

Lin

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

308

280

View full text Add to dashboard Cite

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“…23 Okada et al 24 showed that the accumulation of platelets in preserved and transplanted rat lungs was associated with the degree of reperfusion injury. Platelet adherence also resulted in capillary congestion.…”

Section: Discussionmentioning

confidence: 99%

Soluble P-Selectin and the Risk of Primary Graft Dysfunction After Lung Transplantation

Kawut

Okun

Shimbo

et al. 2009

Chest

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“…Although data from the cardiac surgical literature does suggest an inflammatory effect from cardiopulmonary bypass, there is no evidence to suggest that bypass should be delayed when it is clearly indicated during transplantation (30,(34)(35)(36)(37)(38)(39).…”

Section: Operative and Perioperative Considerations In Lung Transplanmentioning

confidence: 99%

Lung Transplantation for Cystic Fibrosis

Adler

Aurora

Barker

et al. 2009

Proceedings of the American Thoracic Society

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Lung ischemia–reperfusion injury: implications of oxidative stress and platelet–arteriolar wall interactions

Cited by 101 publications

References 190 publications

Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process

Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process

Soluble P-Selectin and the Risk of Primary Graft Dysfunction After Lung Transplantation

Lung Transplantation for Cystic Fibrosis

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