Mechanisms of ventilator-induced lung injury in healthy lungs

Silva, Pedro L.; Negrini, Daniela; Rocco, Patrícia Rieken Macêdo

doi:10.1016/j.bpa.2015.08.004

Cited by 50 publications

(44 citation statements)

References 95 publications

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“…Pulmonary microvascular endothelial cells and alveolar/airway epithelial cells also respond to elevated physical forces and may contribute to VILI. (34) Neutrophils also contribute to the inflammatory response during MV. (35) Although the role of miR-146a in small airway epithelial cells has been investigated in vitro,(23) additional studies should investigate how altering miR-146a expression in other cell types alters VILI.…”

Section: Discussionmentioning

confidence: 99%

“…The current study focused on how microRNAs regulate mechanically induced inflammation during MV and how these mechanical forces can disrupt the alveolar-capillary barrier. (34) Previous studies indicate that modulating cytoskeletal structure and signaling can mitigate barrier disruption(36, 37) and future studies could investigate how microRNAs, which are known to target these pathways, modulate VILI. In vivo, AMs interact directly with the alveolar microenvironment via attachment to alveolar epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

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Nanoparticle delivery of microRNA-146a regulates mechanotransduction in lung macrophages and mitigates lung injury during mechanical ventilation

Bobba

Fei

Shukla

et al. 2019

Preprint

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During mechanical ventilation, injurious biophysical forces exacerbate lung injury. These forces disrupt alveolar capillary barrier integrity, trigger proinflammatory mediator release, and differentially regulate genes and non-coding oligonucleotides such as microRNAs. In this study, we identify miR-146a as a mechanosensitive microRNA in alveolar macrophages that has therapeutic potential to mitigate lung injury during mechanical ventilation. We used humanized in-vitro systems, mouse models, and biospecimens from mechanically ventilated patients to elucidate the expression dynamics of miR-146a that might be required to decrease lung injury during mechanical ventilation. We found that the endogenous increase in miR-146a following injurious was relatively modest and not sufficient to prevent lung injury. However, when miR-146a was highly overexpressed using a nanoparticle-based delivery platform in vivo, it was sufficient to prevent lung injury. These data indicate that the endogenous increase in microRNA-146a during MV is a compensatory response that only partially limits VILI and that nanoparticle delivery approaches that significantly over-express microRNA-146a in AMs is an effective strategy for mitigating VILI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nanoparticle delivery of microRNA-146a regulates mechanotransduction in lung macrophages and mitigates lung injury during mechanical ventilation

Bobba

Fei

Shukla

et al. 2019

Preprint

View full text Add to dashboard Cite

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“…18 A superdistensão regional dos alvéolos causada pela aplicação de grandes volumes ou pressões pode provocar abrasão do epitélio, inativação de surfactante e deformação de células e matriz extracelular. 16,18 Essa deformação cíclica alveolar leva a lesões que geram perturbações proporcionais à frequência, amplitude e duração do estresse tecidual. Estudo demonstrou que a maioria das lesões é iniciada ainda nos primeiros minutos da VM.…”

Section: Discussionunclassified

“…Estudo demonstrou que a maioria das lesões é iniciada ainda nos primeiros minutos da VM. 18 Nesse contexto, o estresse e a tensão sobre o tecido saudável (interleucinas, citocinas, espécies reativas de oxigênio, entre outras) que iniciam uma cascata de eventos que culmina com lesão pulmonar. 3,16,18 Somando-se a isso, a sobrecarga hídrica, relacionada a reposição volêmica excessiva, desorganiza o interstício, contribuindo ainda mais para formação de edema pulmonar severo e LPIV.…”

Section: Discussionunclassified

Papel atual das estratégias ventilatórias protetoras no período perioperatorio: artigo de revisão

et al. 2018

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RESUMOOs fármacos anestésicos utilizados para indução e manutenção de anestesia geral provocam alterações da dinâmica respiratória, fazendo-se necessário o uso de estratégias ventilatórias perioperatórias. A ventilação mecânica, apesar de ser uma terapia de suporte essencial, não é isenta de riscos. Dentre estes, podemos citar complicações pulmonares pós-operatórias (CPPs), que apresentam alta prevalência e potenciais implicações graves. Fatores cirúrgicos, anestésicos e do paciente contribuem para o desenvolvimento de CPPs. Essa revisão faz uma análise de artigos publicados recentemente na literatura sobre ventilação mecânica e suas consequências na morbimortalidade em pacientes cirúrgicos. Por várias décadas e até recentemente, o manejo ventilatório durante cirurgia esteve associado a altos volumes corrente (VC), ausência de pressão expiratória positiva (PEEP) e altas frações inspiradas de oxigênio (FiO 2 mecânica, por meio de estudos experimentais, observacionais e randomizados, indicam a necessidade de se instituir estratégias ventilatórias protetoras perioperatórias. Estas estratégias incluem, de maneira geral, a utilização de baixos VC, uso de PEEP, manobras de recrutamento alveolar e baixa FiO 2 . ABSTRACTThe use of anesthetic drugs for induction and maintenance of general anesthesia cause changes in respiratory dynamics, making it necessary to use perioperative ventilatory strategies. Mechanical ventilation, although it is an essential supportive therapy, is not without risk. Among these, they can mention postoperative pulmonary complications (PPCs), which have high prevalence and potential for serious implications. Many factors such as surgical, anesthetic and patient ones contribute to the development of PPCs. This review analyzes updated published literature on mechanical ventilation and its consequences on morbidity and mortality in surgical patients. For several decades and until recently, ventilatory management during surgery was linked with high tidal volumes (TV), absence of positive expiratory pressure (PEEP) and high inspired oxygen fractions (FiO 2 ). Increasing advances in the understanding of physiopathology of mechanical ventilation-induced lung injury through experimental, observational, and randomized studies indicate a need to institute perioperative protective ventilation. These strategies generally include the use of low CV, use of PEEP, alveolar recruitment maneuvers and low FiO 2 .

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“…This type of change was represented in the upper parts of the lungs (bearing in mind that during mechanical ventilation experimental animals were in a supine position). This suggests that the applied airway pressure may be ideal for opening and ventilation of some lung units, insufficient to open the largest part of the atelectatic zone and cause excessive distension in areas with satisfactory compliance (Gattinoni L et al, 1993;Rimensberger PC et al, 1999;Silva PL et al, 2015). The positive end-expiratory pressure (PEEP) applied during mechanical ventilation in LPV group prevented the formation of significant edema of perivascular, interstitial and alveolar space, which is accompanied by low expressed cellular presence in them.…”

Section: # Paco2 -The Partial Pressure Of Carbon Dioxide In Arterial mentioning

confidence: 99%

Comparative analysis of changes in the lungs of experimental animals’ induced conventional and lung protective ventilation

Videnović

Mladenović²,

Videnovic³

et al. 2018

J Hellenic Vet Med Soc

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Mechanical ventilation has long been the leader in the treatment of critically ill and injured patients in an intensive care unit. The aim of this study was to examine the impact of the application of positive end-expiratory pressure on histopathological findings and on the parameters of ventilation, oxygenation and acid-base status. The experimental study included 42 animals (piglets), which were divided into of tree groups, each containing 14. The animals of the control group (conventional ventilation) were ventilated with the tidal volume of 10-15 mL/kg. Tidal volume of 6 mL/kg was applied in the low tidal ventilation group, whereas the ventilation strategy in the lung protective ventilation group meant the application of a tidal volume of 6 mL/kg and the 7 mbar of positive end-expiratory pressure. Mechanical ventilation in each animal lasted for 4 hours. After conducting mechanical ventilation, samples were taken from the lung tissue, which were sent for histopathological examination. The parameters of ventilation, oxygenation and acid-base status were measured after each hour’s duration of mechanical ventilation. Application of positive end-expiratory pressure 5-10 mbar during mechanical ventilation is a safe and useful method which is not followed by the occurrence of significant abnormalities in the structure of the ventilated lung. However, a low tidal volume without positive end-expiratory pressure causes significant changes in the histological structure of healthy lungs. Positive end-expiratory pressure keeps the alveoli open throughout the respiratory cycle which allows the lungs to maintain homeostasis in terms of adequate ventilation, oxygenation and acid-base status.

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Mechanisms of ventilator-induced lung injury in healthy lungs

Cited by 50 publications

References 95 publications

Nanoparticle delivery of microRNA-146a regulates mechanotransduction in lung macrophages and mitigates lung injury during mechanical ventilation

Nanoparticle delivery of microRNA-146a regulates mechanotransduction in lung macrophages and mitigates lung injury during mechanical ventilation

Papel atual das estratégias ventilatórias protetoras no período perioperatorio: artigo de revisão

Comparative analysis of changes in the lungs of experimental animals’ induced conventional and lung protective ventilation

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