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The role and mechanism of R-spondin3 in pulmonary vascular barrier dysfunction induced by mechanical ventilation

ABSTRACT: The role and mechanism of R-spondin3 in pulmonary vascular barrier dysfunction induced by mechanical ventilation

PROVIDER: PRJNA941821 | ENA |

REPOSITORIES: ENA

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The role and mechanism of R-spondin3 in pulmonary vascular barrier dysfunction induced by mechanical ventilation

Project description:To investigate the effect of lowl tidal volume (LV) ventilation on the pathological development of severe lung injury, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to influence LV-induced lung injury. A mouse model of septic lung injury induced by cecal ligation and puncture was conducted, 24 h post-CLP,mice were exposed to LV (6ml/kg) for 12h

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Impact of aging on pulmonary cellular responses during mechanical ventilation

Project description:Acute respiratory distress syndrome (ARDS) results in significant morbidity and mortality, especially in the elderly. Mechanical ventilation, a common supportive treatment for ARDS, is necessary for maintaining gas exchange, but can also propagate injury. We hypothesized that aging would exacerbate the pathophysiological responses to mechanical ventilation. Young and aged male mice were mechanically ventilated and changes in surfactant function, inflammation, and vascular permeability were assessed. Additionally, single-cell RNA sequencing was used to delineate cell-specific transcriptional changes. The results showed that surfactant dysfunction was augmented in aged mice, while inflammation was less pronounced in aged animals. Futhermore, vascular permeability was significantly increased with aging. Differential gene expression and pathway analyses revealed that aged endothelial cells exhibited altered cell-cell junction formation and that alveolar macrophages in aged mice showed a blunted inflammatory response. These results highlight the complex interplay between aging and mechanical ventilation, including an age-related predisposition to endothelial barrier dysfunction due to altered cell-cell junction formation and decreased inflammation, potentially due to immune exhaustion. It is concluded that age-related vascular changes may underlie the increased susceptibility to injury during mechanical ventilation in elderly patients.

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Effect of mechanical ventilation and mechanical ventilationon with positive end expiratory pressure(PEEP) application on diaphragmatic dysfunction in rabbits

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Impact of aging on pulmonary cellular responses during mechanical ventilation

Project description:Impact of aging on pulmonary cellular responses during mechanical ventilation

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Transcription profiling of lung samples from mouse and rat treated with mechanical ventilation

Project description:This series contain mouse and rat lung samples treated with mechanical ventilation and corresponded controls.

2007-07-20 | E-GEOD-2368 | biostudies-arrayexpress

Age Dependent Gene Expression Responses to Inhaled Lipopolysaccharide Combined with Mechanical Ventilation

Project description:Children have a lower incidence and mortality from acute lung injury than adults, and infections are the most common event associated with acute lung injury (ALI). To study the effects of age on susceptibility to ALI, we investigated the responses to microbial products combined with mechanical ventilation in juvenile (21 day) and adult (16 week-old) mice. We hypothesized that the increased incidence and severity of lung injury associated with increasing age is due in large part to acquired changes in the way in which inflammatory responses are activated in the lungs in response to microbial products and mechanical ventilation. Juvenile (21 day) and adult (16 week) C57BL/6 mice were treated with an aerosol of E. coli 0111:B4 lipopolysaccharide (LPS) (20 mL of 0.1 mg/mL) for 30 minutes in a sealed aerosol chamber, immediately followed by mechanical ventilation (LPS+MV) using tidal volume = 15 mL/kg, rate = 80 breaths/min, FiO2 = 30% and positive end expiratory pressure = 2 cm H2O for the duration of the study period time = 2 hours. Comparison groups included mice treated with LPS or mechanical ventilation (MV) alone, and untreated age-matched controls. There were N = 4 animals per group except the juvenile mice treated with MV alone and LPS+MV where there were N = 3. Each sample was an individual animal, therefore there were 30 samples. Mice treated with LPS alone were placed into a sealed aerosol chamber as stated above, and then allowed to breath spontaneously with free access to food and water for the duration of the study period time = 2 hours. Mice treated with MV alone were treated with the mechanical ventilation protocol stated above for the duration of the study period time = 2 hours. At the end of the study period, the mice were euthanized, and the lungs were immediately removed and placed into RNAlater (Ambion, Austin, TX) for at least 24 hr prior to isolation of total lung mRNA.

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Mechanical Ventilation Augments LPS-induced Lung Injury

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Effect of intra-operative mechanical ventilation on plasma proteomics and biomarkers of inflammation and vascular injury

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