Rat Ards Model
Rat Ards Model - Related Videos
07:20
Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)
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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
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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.
09:39
Creation of Reversible Cholestatic Rat Model
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2011
Cholestasis is a clinical condition commonly encountered by both surgeons and gastroenterologists. Creation of a reversible cholestatic rat model can be challenging in view of the smaller size and unique hepatopancreatobiliary anatomy in rats. This video article demonstrates the creation of a reversible cholestatic model.
02:36
Generating a Glioblastoma Rat Model
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2025
Source: Bolcaen, J., et. al., PET and MRI Guided Irradiation of a Glioblastoma Rat Model Using a Micro-irradiator. J. Vis. Exp. (2017)This video demonstrates the procedure for establishing a glioblastoma rat model by stereotactically injecting brain tumor-causing glioblastoma cells into the prefrontal cortex.
08:18
A Model of Chronic Nutrient Infusion in the Rat
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Cited by 1 •
2013
A protocol for chronic infusions of glucose and Intralipid in rats is described. This model can be used to study the impact of nutrient excess on organ function and physiological parameters.
FAQs
Pulmonary inflammation can weaken the alveolar-capillary barrier, allowing fluid to accumulate in lung tissue and alveolar spaces. This edema interferes with efficient gas exchange and contributes to the physiological abnormalities associated with acute respiratory distress syndrome. Measuring inflammatory, structural, and functional responses together helps researchers connect molecular changes with diffuse alveolar damage rather than interpreting any single finding in isolation.
Inflammatory insults, aspiration, infection-related stimuli, and mechanical ventilation do not reproduce identical injury pathways. Each can emphasize different aspects of inflammation, barrier disruption, edema, or impaired gas exchange. Consequently, the selected induction method should match the biological question, and investigators must characterize the resulting model before concluding that its responses represent the feature of ARDS under study.
Mechanical ventilation can serve as a controlled insult for producing lung injury, allowing investigators to examine how ventilation-associated conditions influence pulmonary responses. Its effects should be interpreted alongside physiological, histological, and molecular measurements because ventilation-related injury may not reproduce every feature generated by inflammation, aspiration, or infection-related stimuli. This comparison supports more precise model selection.
A typical evaluation begins with a controlled insult, followed by assessment of the lungs at physiological, histological, and molecular levels. Physiological measurements indicate functional impairment, histology reveals structural injury such as diffuse alveolar damage, and molecular analyses identify inflammatory or protective responses. Combining these layers provides a more complete characterization of model performance and biological relevance.
Useful outcomes span lung function, tissue structure, and molecular signaling. Physiological findings can indicate impaired gas exchange, histological analysis can document inflammation, edema, and alveolar-capillary disruption, and molecular measurements can reveal candidate biomarkers or protective mechanisms. Concordance among these readouts strengthens interpretation, while disagreement may show that an induction method captures only selected aspects of ARDS.
Researchers may select this system to investigate how diffuse alveolar damage develops, identify biomarkers, examine protective mechanisms, or evaluate potential therapies before clinical studies. Its value depends on matching the induction method and outcome measures to the research question. Careful characterization is essential because no single model necessarily represents every biological feature of human acute respiratory distress syndrome.