Ventilator-Associated Lung Injury

Garfield, Benjamin; Handslip, Rhodri; Patel, Brijesh

doi:10.1016/b978-0-08-102723-3.00237-7

Cited by 5 publications

(4 citation statements)

References 94 publications

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“…Mechanical ventilation (MV) is essential in life support for critically ill patients with acute respiratory distress syndrome (ARDS), but it can also cause or aggravate lung damage due to excessively high stretch (>10% strain) loaded on the airways during treatment, a phenomenon called ventilator-induced lung injury (VILI) [1][2][3][4]. Such high stretch has been reported to induce several pathological responses including pulmonary fibrosis (PF), which is characterized by progressive and irreversible pathogenic airway remodeling involving airway smooth muscle cells (ASMCs) [5][6][7][8][9][10]. For example, young children aged 2 weeks to 3.5 years who were born as early as 23-24 weeks preterm and, thus, required MV show an increased amount of ASMCs in the walls of small airways [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

High Stretch Associated with Mechanical Ventilation Promotes Piezo1-Mediated Migration of Airway Smooth Muscle Cells

Luo,

Gu,

Wang

et al. 2024

IJMS

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Ventilator-induced lung injury (VILI) during mechanical ventilation (MV) has been attributed to airway remodeling involving increased airway smooth muscle cells (ASMCs), but the underlying mechanism is not fully understood. Thus, we aimed to investigate whether MV-associated high stretch (>10% strain) could modulate mechanosensitive Piezo1 expression and thereby alter cell migration of ASMCs as a potential pathway to increased ASMCs in VILI. C57BL/6 mice and ASMCs were subjected to MV at high tidal volume (VT, 18 mL/kg, 3 h) and high stretch (13% strain, 0.5 Hz, 72 h), respectively. Subsequently, the mice or cells were evaluated for Piezo1 and integrin mRNA expression by immunohistochemical staining and quantitative PCR (qPCR), and cell migration and adhesion by transwell and cell adhesion assays. Cells were either treated or not with Piezo1 siRNA, Piezo1-eGFP, Piezo1 knockin, Y27632, or blebbistatin to regulate Piezo1 mRNA expression or inhibit Rho-associated kinase (ROCK) signaling prior to migration or adhesion assessment. We found that expression of Piezo1 in in situ lung tissue, mRNA expression of Piezo1 and integrin αVβ1 and cell adhesion of ASMCs isolated from mice with MV were all reduced but the cell migration of primary ASMCs (pASMCs) isolated from mice with MV was greatly enhanced. Similarly, cell line mouse ASMCs (mASMCs) cultured in vitro with high stretch showed that mRNA expression of Piezo1 and integrin αVβ1 and cell adhesion were all reduced but cell migration was greatly enhanced. Interestingly, such effects of MV or high stretch on ASMCs could be either induced or abolished/reversed by down/up-regulation of Piezo1 mRNA expression and inhibition of ROCK signaling. High stretch associated with MV appears to be a mechanical modulator of Piezo1 mRNA expression and can, thus, promote cell migration of ASMCs during therapeutic MV. This may be a novel mechanism of detrimental airway remodeling associated with MV, and, therefore, a potential intervention target to treat VILI.

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Section: Introductionmentioning

confidence: 99%

High Stretch Associated with Mechanical Ventilation Promotes Piezo1-Mediated Migration of Airway Smooth Muscle Cells

Luo,

Gu,

Wang

et al. 2024

IJMS

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“…La ventilación mecánica (VM) es una estrategia fundamental en el manejo del paciente críticamente enfermo en la unidad de cuidados intensivos (UCI), sin embargo puede ser deletérea 1 . Una de las estrategias para evitar una lesión pulmonar inducida por VM es la programación de un volumen tidal (VT) bajo, basado en el peso ideal (PI) del paciente 2 . Generalmente, valores entre 8 ml/kg y 6 ml/kg de PI son aceptables en la mayoría de los contextos clínicos 3 .…”

Section: Introductionunclassified

Precisión de la programación de volumen tidal mediante fórmulas de estimación de estatura

Acosta-Tovar,

Cervantes-Araujo,

Rojas-Trejo

et al. 2024

REIE

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Para programar la ventilación mecánica debe conocerse el peso ideal del paciente, que se calcula a partir de su talla. Sin embargo, no puede colocarse en bipedestación para utilizar un estadímetro, por lo que deben usarse métodos de estimación de estatura. Una mala programación puede generar el desarrollo de lesión pulmonar inducida por aumento de volumen tidal. Objetivo: Analizar la diferencia del cálculo de volumen tidal basado en el peso ideal calculado a partir de índices de estimación de estatura, comparado con el volumen tidal basado en el peso ideal calculado a partir de la estatura real en población sana en México. Método: Los datos fueron obtenidos de una muestra total de 246 personas con una edad mayor a 18 y menor a 30 años. El 54.48% ( 134) son mujeres y el 45.52% (112) son hombres. Para realizar las mediciones antropométricas se utilizó un estadímetro marca Seca modelo 213 y una cinta métrica Seca 201. Los datos se analizaron en el programa IBM SPSS statistics V21 x64. Resultados: El volumen tidal a 6 ml/kg de peso ideal fue de 378.76 ± 39.88 y a 8 ml/kg de peso ideal fue de 505.01 ± 53.17 en la población en general. Conclusiones: El cálculo de talla, peso ideal y volumen tidal realizado con el método de Chumlea y media brazada da un resultado distinto al método de referencia (estadímetro). Los métodos no son equivalentes para la determinación de la talla y los cálculos derivados.

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“…However, even though the protective ventilation strategy (limited tidal volume, plateau pressure, and PEEP) has been widely applied in clinical practice, it remains difficult to reduce VILI and ARDS mortality. Therefore, for mechanically ventilated ARDS patients who are perceived to be at the highest risk of death, rescue strategies such as extracorporeal membrane oxygenation, inhaled nitric oxide, prone positioning, and high frequency oscillatory ventilation are often considered, but there is no therapeutic drug to prevent or cure it, suggesting that the underlying mechanism of VILI still needs to be unraveled [ 6 , 9 , 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Mechanical Ventilation-Related High Stretch Mainly Induces Endoplasmic Reticulum Stress and Thus Mediates Inflammation Response in Cultured Human Primary Airway Smooth Muscle Cells

Yang

Guo

et al. 2023

IJMS

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Ventilator-induced lung injury (VILI) occurs in mechanically ventilated patients of respiratory disease and is typically characterized by airway inflammation. However, recent studies increasingly indicate that a major cause of VILI may be the excessive mechanical loading such as high stretch (>10% strain) on airway smooth muscle cells (ASMCs) due to mechanical ventilation (MV). Although ASMCs are the primary mechanosensitive cells in airways and contribute to various airway inflammation diseases, it is still unclear how they respond to high stretch and what mediates such a response. Therefore, we used whole genome-wide mRNA-sequencing (mRNA-Seq), bioinformatics, and functional identification to systematically analyze the mRNA expression profiles and signaling pathway enrichment of cultured human ASMCs exposed to high stretch (13% strain), aiming to screen the susceptible signaling pathway through which cells respond to high stretch. The data revealed that in response to high stretch, 111 mRNAs with count ≥100 in ASMCs were significantly differentially expressed (defined as DE-mRNAs). These DE-mRNAs are mainly enriched in endoplasmic reticulum (ER) stress-related signaling pathways. ER stress inhibitor (TUDCA) abolished high-stretch-enhanced mRNA expression of genes associated with ER stress, downstream inflammation signaling, and major inflammatory cytokines. These results demonstrate in a data-driven approach that in ASMCs, high stretch mainly induced ER stress and activated ER stress-related signaling and downstream inflammation response. Therefore, it suggests that ER stress and related signaling pathways in ASMCs may be potential targets for timely diagnosis and intervention of MV-related pulmonary airway diseases such as VILI.

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Ventilator-Associated Lung Injury

Cited by 5 publications

References 94 publications

High Stretch Associated with Mechanical Ventilation Promotes Piezo1-Mediated Migration of Airway Smooth Muscle Cells

High Stretch Associated with Mechanical Ventilation Promotes Piezo1-Mediated Migration of Airway Smooth Muscle Cells

Precisión de la programación de volumen tidal mediante fórmulas de estimación de estatura

Mechanical Ventilation-Related High Stretch Mainly Induces Endoplasmic Reticulum Stress and Thus Mediates Inflammation Response in Cultured Human Primary Airway Smooth Muscle Cells

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