Ventilation Induced Lung Injury
Ventilation Induced Lung Injury - Related Videos
07:55
Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice
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Cited by 7 •
2011
A murine model for ventilator induced lung injury is an important tool to study an acute lung injury in vivo. Here, we report an easy applicable in situ model for acute lung injury using high-pressure mechanical ventilation to induce acute failure of the lung.
04:10
Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents
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2025
In this study, a non-invasive endotracheal instillation technique is demonstrated to develop ALI in rats using a basic laryngoscope to ensure precise LPS delivery to the lungs. The LPS is instilled via an endotracheal tube using a laryngoscope. The magnitude of lung injury is evaluated at multiple time points.
02:38
Lipopolysaccharide-Induced Acute Lung Injury in Mice for Exosome and Immune Analysis
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2026
Source: Yuan, Z., et al. Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury. J. Vis. Exp. (2018)This video demonstrates an in vivo mouse model for inducing and analyzing acute lung injury (ALI) using intraperitoneal administration of bacterial lipopolysaccharide. The inflammatory cascade triggered by alveolar macrophages and neutrophils leads to epithelial and endothelial barrier disruption, allowing fluid and immune cells to accumulate in the alveoli. Alveolar...
08:58
Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs
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2025
This protocol describes the development of a neonatal piglet model of acute lung injury that models early pathogenic events occurring in the preterm lung, including sub-adequate surfactant quantity, hyperoxia, high-pressure ventilation, and inflammation, to facilitate understanding of molecular triggers of bronchopulmonary dysplasia and enhance therapeutic translation.
10:02
Characterization of the Isolated, Ventilated, and Instrumented Mouse Lung Perfused with Pulsatile Flow
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Cited by 12 •
2011
The following protocol outlines the process of isolating, ventilating and instrumenting mouse lungs to measure steady or pulsatile pulmonary vascular pressure-flow relationships in order to quantify the effects of blood flow, airflow, airway changes and vascular changes on right ventricular afterload.
FAQs
Unstable alveoli may collapse during one part of the breathing cycle and reopen during another. Repeated movement creates shear stress at the alveolar surfaces, adding mechanical damage even when the primary problem is respiratory failure. This process can disrupt the alveolar-capillary barrier, promoting edema and worsening gas exchange. Preventing excessive cycling is therefore a central lung-protective goal.
Excessive tidal volume stretches lung units beyond a tolerable range, causing overdistension, while excessive airway pressure adds mechanical stress to the ventilated lung. Together, these forces can injure alveolar structures and disrupt the alveolar-capillary barrier. The resulting edema can impair gas exchange, making control of both volume and pressure clinically important.
Mechanical injury can activate inflammation within the lung, rather than remaining a purely local mechanical problem. Inflammatory signaling may increase pulmonary damage and contribute to disruption of the alveolar-capillary barrier. Mediators associated with this response can also produce systemic inflammatory effects, which helps explain why severe ventilation-related injury may affect organs beyond the lungs.
Positive end-expiratory pressure must be selected for the individual patient because unstable alveoli are vulnerable to repeated collapse and reopening. An appropriate individualized level can help limit that cycle while supporting adequate oxygenation. The goal is not simply to apply pressure, but to coordinate end-expiratory support with controlled ventilation, alveolar stability, and the patient’s oxygenation needs.
A lung-protective approach begins by choosing an appropriate tidal volume, controlling airway pressures, and setting positive end-expiratory pressure for the individual patient. These elements address different contributors to injury: volume limits overdistension, pressure control reduces excessive mechanical stress, and individualized end-expiratory support helps address unstable alveoli. Adequate oxygenation remains an essential outcome during this process.
Clinicians should consider ventilation-induced lung injury when mechanically ventilated patients with respiratory failure develop or risk worsening pulmonary injury. The concern is especially relevant when ventilation exposes the lung to excessive pressure or volume, or when unstable alveoli repeatedly open and close. Applying protective settings in this context aims to reduce additional damage while preserving adequate oxygenation.
Treatment success cannot be judged only by whether a patient remains connected to a ventilator. Clinicians also need to consider whether ventilation is maintaining adequate oxygenation without promoting edema, worsening gas exchange, or amplifying systemic inflammation. These outcomes connect ventilator management with the patient’s broader clinical course and with potential effects on other organs.