Effect of lung ischemia–reperfusion on oxidative stress parameters of remote tissues

Eşme, Hıdır; Fidan, Hüseyin; Köken, Tülay; Solak, Okan

doi:10.1016/j.ejcts.2005.12.008

Cited by 47 publications

(37 citation statements)

References 21 publications

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“…They overwhelm the lung's antioxidant defense system to the detriment of cellular metabolic function and signaling, most especially in the mitochondria of the endothelium and alveolar macrophages (see below). Ultimately, IR in the lung causes systemic effects by inducing heart and liver injury due to activated neutrophils and the significant amount of ROS that is produced (60).…”

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

303

270

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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

303

270

View full text Add to dashboard Cite

show abstract

“…The rabbit a rodent to be larger and easier handling was considered appropriate for this research [9][10][11][12][13][14][15][16][17][18][19][20][21] . To these factors is associated with ease of anesthesia protocol, which provided adequate hypnosis and analgesia, an anesthetic for up to 60 minutes.…”

Section: Discussionmentioning

confidence: 99%

“…Because of the systemic inflammatory response, the I/R injury liver induces the production of reactive oxygen species (ROS) whose distance deleterious effects may be more deleterious than local effects 11,12 .…”

Section: Introductionmentioning

confidence: 99%

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The role of N-acetyl-cysteine in the lung remote injury after hepatic ischemia and reperfusion in rabbits

Castro

Lauz

et al. 2012

Acta Cir. Bras.

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PURPOSE:To study the lesions in the lung of rabbits caused by ischemia/reperfusion hepatic (I/R) after the use of N-acetyl-cysteine (NAC). METHODS: Twenty-four rabbits distributed in two groups: control group GI (n = 12) 5% glucose solution and experiment group GII (n = 12) NAC. The animals were pre-anesthetized with 1% acepromazine maleate and anesthetized with ketamine 10% and 2% xylazine intramuscularly. The GI and GII were given glucose solution intravenously or NAC 15min before occlusion of the hepatic pedicle (30 min). After the period of reperfusion of 24h (n = 6) or 48h (n = 6), liver and lung samples were collected for histology and immunohistochemistry to assess the impairment of cell. RESULTS:The animals of GII and GII-24h-48h showed parenchyma liver close to normal, when using NAC. The GII and GII-24h-48h showed lower thickness of alveolar cells that GI and GI-24h-48h. The expression of caspase 3 in lung cells GII presented smaller value compared to the GI group. CONCLUSION: N-acetyl-cysteine administered 15min prior to the injury ischemia/reperfusion had a significant protective role by minimizing lung injury and apoptotic morphology in the period observed. Key words: Acetylcysteine. Lung. Reperfusion. Ischemia. Liver. Rabbits. RESUMO OBJETIVO:Estudar as lesões no fígado e no pulmão de coelhos, provocadas pela isquemia/reperfusão hepática (I/R) moduladas pelo uso da N-acetil-cisteína (NAC). MÉTODOS: Vinte e quatro coelhos distribuídos em dois grupos: Grupo controle GI (n=12) solução de glicose 5% e Grupo experimento GII (n=12) NAC. Os animais foram pré-anestesiados com maleato de acepromazina 1% e anestesiados com cloridrato de quetamina 10% e xilazina 2% via intramuscular. Os grupos GI e GII receberam solução glicosada ou NAC respectivamente via endovenosa 15min antes da oclusão do pedículo hepático (30 min). Após iniciou-se o período de reperfusão por 24h (n=6) ou 48h (n=6), terminada a reperfusão, amostras do fígado e pulmão foram coletadas para a histologia e imunoistoquímica para avaliar o comprometimento celular. RESULTADOS: Os animais do grupo GII-24h e GII-48h apresentaram arquitetura do parênquima hepático próximo do normal, quando se utilizou NAC. Os grupos GII-24h e GII-48h apresentaram menor espessura das células alveolares que os grupos GI-24h e GI-48h. A expressão da caspase 3 nas células pulmonares do grupo GII, apresentou valor menor comparada ao grupo GI. CONCLUSÃO: A N-acetil-cisteína administrada 15min prévios a lesão da isquemia/reperfusão teve um papel protetor significativo minimizando as lesões morfológicas e apoptóticas pulmonares nos períodos observados. Descritores: Acetilcisteína. Pulmão. Reperfusão. Isquemia. Fígado. Coelhos.

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“…17,18 These factors can cause oxidative damage to lung tissues, increasing alveolar endothelium permeability and infiltration of inflammatory cells, edema, impairing intrapulmonary shunt fraction and ventilation perfusion. Administration of anti-inflammatory molecules, including corticosteroids and serine protease inhibitor aprotinin, can reduce the lung damage resulting from CPB-induced I/R injury, [19][20][21][22][23] though the molecular mechanisms underlying CPB-induced lung injury remain unclear.…”

mentioning

confidence: 99%

Human amniotic mesenchymal stem cells alleviate lung injury induced by ischemia and reperfusion after cardiopulmonary bypass in dogs

Qiang

Liang

2016

Laboratory Investigation

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Transplantation of mesenchymal stem cells may inhibit pathological immune processes contributing to ischemia/ reperfusion (I/R) injury. This study aimed to assess the capacity of human amniotic MSC (hAMSCs) to ameliorate I/R injury in a dog model of cardiopulmonary bypass (CPB). Dissociated hAMSCs were cultured ex vivo, and their immunophenotypes were assessed by flow cytometry and immunohistochemistry. A dog model of CPB was established by surgical blockage of the aorta for 1 h. Dogs either underwent mock surgery (Sham group), CPB (model group), or CPB, followed by femoral injection of 2 × 10 7 hAMSCs (n = 6). Anti-human nuclei staining revealed hAMSCs in the lungs 3 h after surgery. Oxygen index (OI) and respiratory index (RI) of arterial blood were measured using a biochemical analyzer. Venous blood TNF-α, IL-8, MMP-9, and IL-10 concentrations were measured by ELISA. Pathological changes in the lung were assessed by light microscopy. Third-generation-cultured hAMSCs expressed high levels of CD29, CD44, CD49D, CD73, and CD166 levels, but low CD34 or CD45 amounts and their cytoplasm contained Vimentin. In CPB model animals, OI was elevated and RI reduced; TNF-α, IL-8, and MMP-9 levels were elevated, and IL-10 levels reduced within 3h (Po0.05), but hAMSC transplantation significantly ameliorated these changes (Po0.05). Pathological changes observed in the hAMSC group were significantly less severe than those in the CPB group. In conclusion, hAMSC transplantation can downregulate proinflammatory factors and reduce MMP-9 levels, whereas upregulating the anti-inflammatory molecule IL-10, thus reducing I/R lung injury in a dog model of CPB.

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Effect of lung ischemia–reperfusion on oxidative stress parameters of remote tissues

Cited by 47 publications

References 21 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

The role of N-acetyl-cysteine in the lung remote injury after hepatic ischemia and reperfusion in rabbits

Human amniotic mesenchymal stem cells alleviate lung injury induced by ischemia and reperfusion after cardiopulmonary bypass in dogs

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