Introduction to the VILI Animal Model

The animal model of ventilator-induced lung injury (VILI) is a classic experimental paradigm used to mimic the pulmonary damage resulting from alveolar overdistension and repeated collapse during mechanical ventilation. Typically, after anesthetizing the animal and establishing tracheal intubation, parameters such as high tidal volume, elevated airway pressure, or low positive end-expiratory pressure are set on the mechanical ventilator and maintained for a specified duration to induce lung tissue injury.

Following model establishment, disruption of the alveolar epithelial–capillary endothelial barrier, decreased lung compliance, and pulmonary edema may occur, accompanied by pathological changes such as inflammatory cell infiltration, release of pro-inflammatory cytokines (e.g., TNF-α, IL-6), and enhanced oxidative stress. This model is widely employed in studies of the pathogenesis of acute lung injury/ARDS, as well as in the in vivo evaluation of lung‑protective ventilation strategies and anti‑inflammatory agents.

Advantages of Aniphe BioLab’s VILI Animal Model Platform Services

Aniphe BioLab‑mechanical ventilation–induced lung injury (VILI) animal model platform, centered on precise control of ventilatory parameters and the ability to establish a stable lung injury phenotype, provides a reliable in vivo model system for investigating the mechanisms of acute lung injury and evaluating lung‑protective strategies.

	The multi-parameter ventilation protocol is well-established. It supports multiple ventilation modes, including tidal volume, high airway pressure, and low PEEP, to meet the research needs of varying degrees of lung injury.
	Ventilation conditions are precisely controllable. Reproducible lung injury is induced through precise modulation of respiratory rate, tidal volume, and pressure parameters.
	The model exhibits high stability. Standardize anesthesia, intubation, and ventilation protocols to minimize procedural variability and enhance batch-to-batch consistency.
	Pathological features closely resemble clinical findings. It can reliably reproduce typical VILI manifestations, including alveolar overdistension, recurrent collapse, and pulmonary edema.
	The inflammatory response is reproducible. It can induce inflammatory cell infiltration and a significant increase in pro-inflammatory cytokines such as TNF-α and IL-6.
	The multi-dimensional evaluation system has been refined. Systematic analysis was achieved by integrating pulmonary compliance measurements, blood gas analysis, and histopathological evaluation.

Modeling cycle	1–2 weeks
Laboratory animals	Adult SD rats, C57BL/6 mice, or New Zealand rabbits
Positive drug	Dexamethasone (anti-inflammatory), ulinastatin (protease inhibitor), N-acetylcysteine (antioxidant), pulmonary surfactant, and others are used to assess the model’s responsiveness to lung-protective strategies.
Application areas	Pathogenesis of VILI (barotrauma, volutrauma, biotrauma, and barrier disruption); evaluation of protective ventilation strategies; screening of anti-inflammatory/antioxidant lung‑protective agents; investigation of ECMO‑related lung injury and weaning strategies.

Construction of an Animal Model of Ventilator-Induced Lung Injury

In the experiment, after anesthesia and tracheal intubation, the animals were connected to a small-animal ventilator. A tidal volume significantly higher than physiological levels was set, and ventilation was maintained for a specified duration; concurrently, a low PEEP or a high inspiratory pressure could be applied to sustain continuous overdistension of the alveoli. This protocol induces alveolar structural damage, increased capillary permeability, and pulmonary interstitial edema.

Following model establishment, animals exhibit decreased pulmonary compliance and impaired gas exchange, accompanied by inflammatory cell infiltration and increased release of pro-inflammatory cytokines. This makes it an important experimental model for investigating the mechanisms of ventilator‑induced lung injury and for developing lung‑protective ventilation strategies.