Ards Mouse Model
Ards Mouse Model - Related Videos
07:20
Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)
0 Views •
Cited by 21 •
2016
Repeated pulmonary lavages in anesthetized pigs induce lung injury resembling major aspects of human acute respiratory distress syndrome (ARDS). For this purpose the lungs are repeatedly lavaged with 0.9% saline at 37 °C. The goal of the protocol is a reproducible mitigation of gas exchange and hemodynamics for research in ARDS.
08:22
The Application of Point-of-Care Ultrasonography (POCUS) in the Management of Acute Respiratory Distress Syndrome (ARDS) in the Intensive Care Unit
0 Views •
2025
Here, we present a protocol for bedside POCUS application in ARDS management within the ICU. It details standardized techniques for lung, cardiac, diaphragm, venous, and gastric assessments to guide ventilation, predict weaning, and prevent complications.
08:12
Invasive Hemodynamic Monitoring of Aortic and Pulmonary Artery Hemodynamics in a Large Animal Model of ARDS
0 Views •
Cited by 5 •
2018
We present a protocol of creating right ventricular dysfunction in a pig model by inducing ARDS. We demonstrate invasive monitoring of left and right ventricular cardiac output using flow probes around the aorta and the pulmonary artery, as well as blood pressure measurements in the aorta and pulmonary artery.
06:24
Mouse Models of Periventricular Leukomalacia
0 Views •
Cited by 28 •
2010
We established mouse models of periventricular leukomalacia (PVL), the predominant brain injury in premature infants characterized by periventricular white matter lesions. Hypoxia/ischemia with/without systemic infection are the primary causes of PVL. Unilateral carotid ligation and hypoxia exposure with/without lipopolysaccharide injection creates PVL-like lesions in P6 mice.
06:22
Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
0 Views •
Cited by 5 •
2021
A combination of surfactant washout using 0.9% saline (35 mL/kg body weight, 37 °C) and high tidal volume ventilation with low PEEP to cause moderate ventilator induced lung injury (VILI) results in experimental acute respiratory distress syndrome (ARDS). This method provides a model of lung injury with low/limited recruitability to study the effect of various ventilation strategies for extended periods.
FAQs
Bacterial components, viral infection, acid aspiration, and mechanical injury can initiate distinct upstream events, but each may activate innate immune pathways in the lung. These pathways promote cytokine release, leukocyte recruitment, and epithelial-endothelial dysfunction. Comparing stimuli helps researchers determine which aspects of respiratory injury arise from the initiating insult and which reflect shared inflammatory mechanisms.
Damage to the alveolar-capillary barrier links inflammation with pulmonary edema and impaired gas exchange. It indicates that immune activation has produced tissue-level consequences beyond cytokine release alone. Measuring this component alongside inflammation allows investigators to assess whether an intervention limits structural lung injury, rather than merely reducing selected molecular or cellular markers.
Infection-based models expose the interaction between a pathogen and the host response, while models using bacterial components or noninfectious injury stimuli can isolate inflammatory and tissue-damage processes without requiring the same infectious context. This comparison helps determine whether respiratory failure is associated primarily with the initiating agent, dysregulated innate immunity, or their combined effects.
The initiating stimulus strongly influences the pattern and intensity of lung injury, including inflammation, barrier disruption, edema, and impaired gas exchange. Experimental comparisons can therefore examine how different insults alter severity and how consistently an intervention performs. Interpreting treatment response requires connecting immune regulation with tissue-level outcomes rather than relying on a single endpoint.
A study generally selects an injury stimulus, induces the pulmonary response, and then evaluates inflammatory and tissue-level changes. Investigators can compare disease severity between experimental conditions and examine cytokine release, leukocyte recruitment, barrier damage, edema, and impaired gas exchange. The workflow supports testing how a defined immune manipulation changes progression or recovery-related outcomes.
The choice depends on the biological question. Viral infection and bacterial components support studies of infection-related or pathogen-associated inflammation, whereas acid aspiration and mechanical injury model noninfectious routes of pulmonary damage. Using more than one stimulus can reveal whether a proposed mechanism or treatment acts broadly across injury contexts or only under a particular initiating condition.
Researchers compare treated and untreated animals after inducing the relevant pulmonary injury, then examine changes in immune and tissue outcomes. Anti-inflammatory strategies can be assessed through cytokine release, leukocyte recruitment, and immune regulation, while antimicrobial approaches can be studied in infection-related settings. Barrier damage, edema, and gas exchange provide additional evidence of functional benefit.