Effect of ischemia reperfusion or hypoxia reoxygenation on lung vascular permeability and resistance

Allison, Ronald C.; Kyle, John C.; Adkins, W. K.; Prasad, V. R.; McCord, JM; Taylor, Aubrey E.

doi:10.1152/jappl.1990.69.2.597

Cited by 80 publications

(32 citation statements)

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“…The increase in PVR is mainly due to the vasoconstriction of the pulmonary precapillary system after lung IR (120). The increase in PVR, together with an increase of vascular permeability, the latter of lesser importance (11), results in pulmonary edema in both ischemia (23) and reperfusion (93). The increase in total and extravascular lung water content causes poor gas exchange and lung mechanics, which leads to a lower arterial oxygen tension (Pa O 2 ) (93), increased peak airway pressure, and an elevated alveolar-arterial oxygen gradient [(A-a)DO 2 ] (166).…”

Section: Ir-induced Physiological Changesmentioning

confidence: 99%

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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

315

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: Ir-induced Physiological Changesmentioning

confidence: 99%

“…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).…”

mentioning

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

315

280

View full text Add to dashboard Cite

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“…Allopurinol is another XOD inhibitor that often has been used to study the enzyme's function and has been shown to effectively attenuate lung reoxygenation injury (1,34,35). However, it has also been shown that oxypurinol, a major metabolite of allopurinol, is a scavenger of the highly reactive hydroxyl radical and of hypochlorous acid.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung

Saitô¹,

Ogawa²,

Minamiya³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Saito, Satoshi, Jun-ichi Ogawa, and Yoshihiro Minamiya. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol 289: L400 -L406, 2005. First published May 6, 2005; doi:10.1152/ajplung.00136.2005.-The pathogenesis of reexpansion pulmonary edema is not yet fully understood. We therefore studied its mechanism in a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 3 h. We then evaluated the production of reactive oxygen species in the lungs using fluorescent imaging and cerium deposition electron microscopic techniques and the incidence of apoptosis using the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. We found that pulmonary reexpansion induced production of reactive oxygen species and then apoptosis, mainly in endothelial and alveolar type II epithelial cells. Endothelial cells and alveolar type I and II epithelial cells in the reexpanded lung were positive for TUNEL and cleaved caspase-3. DNA fragmentation was also observed in the reexpanded lung. In addition, wet-dry ratios obtained with reexpanded lungs were significantly higher than those obtained with control lungs, indicating increased fluid content. All of these effects were attenuated by pretreating rats with a specific xanthine oxidase inhibitor, sodium (Ϫ)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo[1,5-a]-1,3,5-triazine-4(1H)-one. It thus appears that pulmonary reexpansion activates xanthine oxidase in both endothelial and alveolar type II epithelial cells and that the reactive oxygen species produced by the enzyme induce apoptosis among the endothelial and alveolar type I and II epithelial cells that make up the pulmonary water-air barrier, leading to reexpansion pulmonary edema.reactive oxygen species; caspase-3; type II alveolar epithelial cell; reoxygenation REEXPANSION PULMONARY EDEMA (RPE) is a rare complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. Although physicians generally believe that, unlike acute respiratory distress syndrome (ARDS), RPE does not require intensive care, the outcome of RPE is reportedly fatal in 20% of patients (17). Moreover, reexpansion after atelectatic storage for hypothermic preservation of lungs before transplantation may be responsible for postpreservation and postreperfusion lung injury (7).The mechanism responsible for RPE is not fully understood. It has been suggested that after atelectasis the mechanical stresses related to lung inflation may cause RPE (28). This effect has also been mentioned as a contributor to the pathogenesis of postpreservation lung injury (9). In addition, some evidence suggests changes in alveolar surfactant may contribute to RPE (26,31), and a number of investigators have reported that neutrophil accumulation in the lung induced by various chemokines (e.g., IL-8 and monocyte chemoattractant protein-1), chemical mediators, and adhesion molecules (24, 30) plays a major role in ...

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“…This type of injury also occurs in lungs (7-1 1). For volume technique, averaged 0.591 f 0.054 (SEM) and example, Allison et al (12) recently demonstrated that ventila-0.465 f 0.054 (SEM), respectively, and were not altered tion of isolated perfused dog lungs with 95% N2/5% C 0 2 followed by reoxygenation or age. Catalase activity in lung tissue by 95% 0215% COz increased pulmonary vascular resistance and erythrocytes was lower in premature lambs, but there and filtration coefficient.…”

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confidence: 99%

Developmental Differences in Catalase Activity and Hypoxic-Hyperoxic Effects on Fluid Balance in Isolated Lamb Lungs

1993

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ABSTRACT. The effects of hypoxia (95% N2/5% C02)The toxic effects of O2 are mediated by 0 2 metabolites, such followed by hyperoxia (95% 02/5% C 0 2 ) were determined as superoxide anion, hydroxyl radical, hydrogen peroxide, and in isolated lungs of premature (gestational age 128 to 135 singlet O2 (1). In lung cells, several endogenous enzyme systems, d) and full-term (postnatal age 0 to 5 d) lambs perfused including superoxide dismutase, catalase, and glutathione perwith autologous blood (100 mL.min-'. kg body weight-').oxidase, protect against damage from these metabolites. ErythIn full-term lungs, hypoxia-hyperoxia compared with hy-rocytes contain high concentrations of these protective enzymes poxia alone decreased pulmonary artery pressure and in-and therefore may also function as an endogenous defense system creased weight gain and extravascular lung water. In pre-(2). It has been demonstrated in several species that lung antioxmature lungs, the increase in weight gain was greater and idant enzyme levels increase during the last 10 to 15% of gestawas associated with hemorrhage and increased pulmonary tion (3-5). This observation suggests that the lungs of fetuses arterial and peak airway pressures. Papaverine eliminated born prematurely may have an increased susceptibility to O2 reoxygenation-induced differences in pulmonary artery toxicity. pressure, peak airway pressure, and weight gain in bothIn systemic organs, toxic O2 metabolites are thought to mediate age groups. Osmotic reflection coefficients for total protein anoxia-reoxygenation injury resulting from ischemia and reperand albumin, measured by a modification of the filtered fusion (6). This type of injury also occurs in lungs (7-1 1). For volume technique, averaged 0.591 f 0.054 (SEM) and example, Allison et al. (12) recently demonstrated that ventila-0.465 f 0.054 (SEM), respectively, and were not altered tion of isolated perfused dog lungs with 95% N2/5% C 0 2 followed by reoxygenation or age. Catalase activity in lung tissue by 95% 0215% COz increased pulmonary vascular resistance and erythrocytes was lower in premature lambs, but there and filtration coefficient. The increase in filtration coefficient were no age-related differences in superoxide dismutase or was prevented by the xanthine oxidase inhibitor, allopurinol, glutathione peroxidase activities. These results demon-suggesting that O2 radicals derived from xanthine oxidase mestrate that hypoxia-hyperoxia in isolated lamb lungs in-diated the change, as proposed for anoxia-reoxygenation injury creased lung weight due to edema formation in full-term in systemic organs (6). lamb lungs and hemorrhage in premature lamb lungs andThe purposes of the present study were to determine whether that this increase was greater in premature lamb lungs. ventilation with 95% N2/5% 0 2 followed by 95% 0215% C 0 2 We speculate that the weight gain caused by reoxygenation (hypoxia-hyperoxia) altered lung fluid balance in isolated lamb was due to a vasodilation-induced increase in surface area lungs and, if...

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Effect of ischemia reperfusion or hypoxia reoxygenation on lung vascular permeability and resistance

Cited by 80 publications

References 0 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

Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung

Developmental Differences in Catalase Activity and Hypoxic-Hyperoxic Effects on Fluid Balance in Isolated Lamb Lungs

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