Ventilator-induced lung injury (VILI) promotes ischemia/reperfusion lung injury (I/R) and NF-kB antibody attenuates both injuries

Chiang, Chiao–Hsi; Pai, Hsin-I; Liu, Shiou-Ling

doi:10.1016/j.resuscitation.2008.02.028

Cited by 40 publications

(31 citation statements)

References 29 publications

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“…Our VILI model reproduces many features reported in other studies [1][2][3][4]14], including inflammatory responses and structural lung damage. Our results are in agreement with those previously reported showing an inability of endogenous host defenses to increase antioxidant capacity, leading to failure of lung repair mechanism [20].…”

Section: Discussionsupporting

confidence: 78%

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Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model

et al. 2011

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Rationale-Apocynin suppresses the generation of reactive oxygen species (ROS) that are implicated in ventilator-induced lung injury (VILI). We thus hypothesized that apocynin attenuates VILI.Methods-VILI was induced by mechanical ventilation with tidal volume (V t ) of 15 ml/kg in isolated and perfused rat lung. Apocynin was administered in the perfusate at onset of mechanical ventilation. A group ventilated with low V t of 5 ml/kg served as control. Hemodynamics, lung Results-There was an increase in lung permeability and lung weight gain after mechanical ventilation with high V t , compared with low V t . Levels of inflammatory cytokines including interleukin-1b (IL-1b), tumor necrosis factor-alpha (TNF-a), and macrophage inflammatory protein-2 (MIP-2) increased in lung lavage fluids; concentrations of carbonyl, thiobarbituric acid reactive substances, and H 2 O 2 were higher in perfusates and lung lavage fluids, and expression of myeloperoxidase, JNK, p38, and caspase-3 in lung tissue was greater in the high-Vt than in the low-Vt group. Administration of apocynin attenuated these inflammatory responses and lung permeability associated with decreased activation of nuclear factor-κB.Conclusions-VILI is associated with inflammatory responses including generation of ROS, cytokines, and activation of mitogen-activated protein kinase cascades. Administration of apocynin at onset of mechanical ventilation attenuates inflammatory responses and VILI in the isolated, perfused rat lung model.

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Section: Discussionsupporting

confidence: 78%

“…The in situ isolated, perfused lung model has been previously described [14]. Briefly, male Sprague-Dawley rats (SD rat) weighing 250-350 g were anesthetized with intraperitoneal injection of sodium pentobarbital.…”

Section: Animal Preparationmentioning

confidence: 99%

Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model

et al. 2011

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“…Several studies failed to show an increase in tumor necrosis factor alpha or IL-1␤ concentration in BALF or plasma after injurious ventilation strategies. 19,21 On the other hand, some VILI studies, including our own, were able to demonstrate elevated levels of pro-inflammatory cytokines in BALF [22][23][24][25][26] and blood. 26 Furthermore, our results are the first to show up-regulation of H 2 O 2 in BALF, lung tissue, and blood from the left ventricle, supporting a previous study showing a significant increase in serum isoprostane in rats ventilated with high V T compared with low V T .…”

Section: Up-regulation Of Cytokines and Reactive Oxygen Species In Bamentioning

confidence: 74%

“…The lung injury score was scaled and evaluated as described previously. 11,18,19 Statistical Analysis Systat 10.0 (Systat Software, San Jose, California) was used for statistical analysis. The normal (or gaussian) distribution was found in the distribution of values of various parameters in all groups.…”

Section: Lung Histopathologymentioning

confidence: 99%

Spillover of Cytokines and Reactive Oxygen Species in Ventilator-Induced Lung Injury Associated With Inflammation and Apoptosis in Distal Organs

et al. 2014

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BACKGROUND:The mechanism between ventilator-induced lung injury (VILI) and multiple organ injury is unclear. The aim of our study was to investigate the mechanisms of VILI-induced distal organ injury. METHODS: VILI was induced in rat lungs with high tidal volume (V T ) ventilation of 40 mL/kg for 6 h. Rats with low V T ventilation of 6 mL/kg served as controls. Inflammatory and apoptotic indices in lung and distal organs were assessed. RESULTS: VILI increased lung weight, airway pressure, inflammation, and apoptotic pathologic changes without hemodynamic changes. The white blood cell count and the levels of H 2 O 2 , interleukin-1␤ (IL-1␤), tumor necrosis factor alpha, and macrophage inflammatory protein-2 in bronchoalveolar lavage fluid were higher in the VILI group compared with the control group. H 2 O 2 , IL-1␤, and tumor necrosis factor alpha in blood from the left ventricle were up-regulated. H 2 O 2 , IL-1␤, tumor necrosis factor alpha, macrophage inflammatory protein-2, c-Jun N-terminal kinase, p38, nuclear factor kappa B, and caspase-3 in lung, heart, liver, and kidney tissues in the VILI group were up-regulated. Furthermore, the apoptotic score for the kidneys was higher than those for other distal organs in the VILI group. CONCLUSIONS: High V T ventilation induces VILI and is associated with inflammation and apoptosis in distal organs. Up-regulation of reactive oxygen species and cytokines in VILI is associated with systemic inflammatory responses. Kidney tissue appears to be more vulnerable than heart and liver tissues following VILI.

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“…22 Thus, nuclear factor kappa B can be activated by numerous stimuli present during critical illness, including ROS, pro-inflammatory cytokines, endotoxins, viruses, and stretch-related lung injury. 22,23 Interestingly, nuclear factor kappa B is suppressed by the presence of antioxidants. 22 In addition, nuclear factor kappa B stimulation by both stretchrelated injury and hyperoxia induces the release of plasminogen activator inhibitor-1 and tissue factor by the airway and alveolar epithelial cells, endothelial cells, macrophages, and fibroblasts.…”

Section: Overview: Cellular Signaling In Vili and The Role Of Rosmentioning

confidence: 99%

Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients?

Kallet

Branson

2016

Respir Care

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Oxygen is both lifesaving and toxic. Appropriate use of oxygen aims to provide a balance between the two effects. Although local oxygen toxicity to the lung is well accepted, recent evidence has called into question the negative consequences of hyperoxemia in other organ beds. Hyperoxia following cardiac arrest, traumatic brain injury, and stroke has been shown to worsen outcomes. The role of hyperoxemia in mechanically ventilated patients, in the face of non-toxic inspired oxygen concentrations, is less clear. This paper will review the data for and against the use of conservative oxygen targets and the avoidance of hyperoxemia in mechanically ventilated patients. Key words: hyperoxia; hyperoxic acute lung injury; lung protective ventilation; oxygen toxicity; reactive oxygen species; ventilator-induced lung injury. [Respir Care 2016;61(6):801-817.

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Ventilator-induced lung injury (VILI) promotes ischemia/reperfusion lung injury (I/R) and NF-kB antibody attenuates both injuries

Cited by 40 publications

References 29 publications

Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model

Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model

Spillover of Cytokines and Reactive Oxygen Species in Ventilator-Induced Lung Injury Associated With Inflammation and Apoptosis in Distal Organs

Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients?

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