Recurrent Recruitment Manoeuvres Improve Lung Mechanics and Minimize Lung Injury during Mechanical Ventilation of Healthy Mice

Reiss, Lucy Kathleen; Kowallik, Anke; Uhlig, Stefan

doi:10.1371/journal.pone.0024527

Cited by 57 publications

(60 citation statements)

References 60 publications

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“…These data fit with clinical studies which showed that RM had no effect on the level of systemic inflammatory cytokines in critically ill ventilated patients with and without ARDS [58,59]. Other experimental studies even showed a decreased inflammatory response when using RMs [60][61][62]. The cytokine attenuation during a RM could be due to the abolition of VILI as demonstrated by Kozian et al [63 •• ].…”

Section: Recruitment Maneuvers and The Open Lung Conceptsupporting

confidence: 83%

Alveolar Recruitment Maneuvers for One-Lung Ventilation During Thoracic Anesthesia

Tusman

Böhm

Suárez-Sipmann

2014

Curr Anesthesiol Rep

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Especially during thoracic surgery, anesthesiologists have to cope with both the drastic alteration of normal pulmonary physiology and the mechanical stress on the lung tissue induced by ventilation. These problems result from the total collapse of the lung being operated on and the partial collapse of the ventilated other lung. In addition, technical factors inherent to thoracic surgery and the patient's condition potentiate such adverse effects. Traditional ventilatory settings described for thoracic surgery have not led to a decrease in the incidence of hypoxemia or perioperative atelectasis. However, lung recruitment maneuvers and ventilatory strategies are aimed at resolving lung collapse in mechanically ventilated patients, improving lung function, and decreasing the rate of post-operative pulmonary complications directly related to lung collapse. This article summarizes recent evidence for the role that lung recruitment maneuvers play during one-lung ventilation anesthesia.

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Section: Recruitment Maneuvers and The Open Lung Conceptsupporting

confidence: 83%

Alveolar Recruitment Maneuvers for One-Lung Ventilation During Thoracic Anesthesia

Tusman

Böhm

Suárez-Sipmann

2014

Curr Anesthesiol Rep

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“…Animals were investigated in LPS-induced and acid-induced models of ARDS, respectively, as well as cytokine-induced pulmonary inflammation, as described before (10,15). In brief, pulmonary inflammation was induced by intranasal (i.n.)…”

Section: Models and Analysis Of Ardsmentioning

confidence: 99%

Smooth Muscle Cells Relay Acute Pulmonary Inflammation via Distinct ADAM17/ErbB Axes

Dreymueller¹,

Martin²,

Schumacher³

et al. 2014

The Journal of Immunology

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In acute pulmonary inflammation, danger is first recognized by epithelial cells lining the alveolar lumen and relayed to vascular responses, including leukocyte recruitment and increased endothelial permeability. We supposed that this inflammatory relay critically depends on the immunological function of lung interstitial cells such as smooth muscle cells (SMC). Mice with smooth muscle protein-22α promotor-driven deficiency of the disintegrin and metalloproteinase (ADAM) 17 (SM22-Adam17−/−) were investigated in models of acute pulmonary inflammation (LPS, cytokine, and acid instillation). Underlying signaling mechanisms were identified in cultured tracheal SMC and verified by in vivo reconstitution experiments. SM22-Adam17−/− mice showed considerably decreased cytokine production and vascular responses in LPS- or acid-induced pulmonary inflammation. In vitro, ADAM17 deficiency abrogated cytokine release of primary SMC stimulated with LPS or supernatant of acid-exposed epithelial cells. This was explained by a loss of ADAM17-mediated growth factor shedding. LPS responses required ErbB1/epidermal growth factor receptor transactivation by TGFα, whereas acid responses required ErbB4 transactivation by neuregulins. Finally, LPS-induced pulmonary inflammation in SM22-Adam17−/− mice was restored by exogenous TGFα application, confirming the involvement of transactivation pathways in vivo. This highlights a new decisive immunological role of lung interstitial cells such as SMC in promoting acute pulmonary inflammation by ADAM17-dependent transactivation.

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“…Ventilation of Nrf2 2/2 and Nrf2 1/1 mice was performed with the flexiVent ventilator (SCIREQ, Montreal, Canada) as described (33) with pressure of 8 cm H 2 O and f = 180/min or 16 cm H 2 O and f = 80/min, FI O 2 = 0.3, and positive end-expiratory pressure = 2 cm H 2 O. Lung mechanics were followed by the forced oscillation technique.…”

Section: In Vivo Ventilationmentioning

confidence: 99%

Interplay between Nuclear Factor Erythroid 2–Related Factor 2 and Amphiregulin during Mechanical Ventilation

Reiss

Fragoulis

Siegl

et al. 2014

Am J Respir Cell Mol Biol

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Mechanical ventilation (MV) elicits complex and clinically relevant cellular responses in the lungs. The current study was designed to define the role of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a major regulator of the cellular antioxidant defense system, in the pulmonary response to MV. Nrf2 activity was quantified in ventilated isolated perfused mouse lungs (IPL). Regulation of amphiregulin (AREG) was investigated in BEAS-2B cells with inactivated Nrf2 or Keap1, the inhibitor of Nrf2, using a luciferase vector with AREG promoter. AREG-dependent Nrf2 activity was examined in BEAS-2B cells, murine precision-cut lung slices (PCLS), and IPL. Finally, Nrf2 knockout and wild-type mice were ventilated to investigate the interplay between Nrf2 and AREG during MV in vivo. Lung functions and inflammatory parameters were measured. Nrf2 was activated in a ventilation-dependent manner. The knockdown of Nrf2 and Keap1 via short hairpin RNA in BEAS-2B cells and an EMSA with lung tissue revealed that AREG is regulated by Nrf2. Conversely, AREG application induced a significant Nrf2 activation in BEAS-2B cells, PCLS, and IPL. The signal transduction of ventilation-induced Nrf2 activation was shown to be p38 MAP kinase-dependent. In vivo ventilation experiments indicated that AREG is regulated by Nrf2 during MV. We conclude that Areg expression is regulated by Nrf2. During high-pressure ventilation, Nrf2 becomes activated and induces AREG, leading to a positive feedback loop between Nrf2 and AREG, which involves the p38 MAPK and results in the expression of cytoprotective genes.

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Recurrent Recruitment Manoeuvres Improve Lung Mechanics and Minimize Lung Injury during Mechanical Ventilation of Healthy Mice

Cited by 57 publications

References 60 publications

Alveolar Recruitment Maneuvers for One-Lung Ventilation During Thoracic Anesthesia

Alveolar Recruitment Maneuvers for One-Lung Ventilation During Thoracic Anesthesia

Smooth Muscle Cells Relay Acute Pulmonary Inflammation via Distinct ADAM17/ErbB Axes

Interplay between Nuclear Factor Erythroid 2–Related Factor 2 and Amphiregulin during Mechanical Ventilation

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