Animal models of acute lung injury

Medical Research Service of the Veterans Affairs/Puget Sound Health Care System, 815 Mercer St., Seattle, WA 98109, USA.
AJP Lung Cellular and Molecular Physiology (Impact Factor: 4.08). 08/2008; 295(3):L379-99. DOI: 10.1152/ajplung.00010.2008
Source: PubMed


Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.

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    • "Acute respiratory distress syndrome (ARDS) is a critical syndrome consisting of acute respiratory failure associated with extensive pulmonary infiltrates[2]. The pathological characterization of ARDS includes injury to the alveolar capillary barrier that leads to the influx of protein-rich fluid into alveolar spaces and subsequent devastating lung fibrosis345. Although extensive studies have investigated the basic mechanisms responsible for the development of IPF and ARDS, no specific pharmacological treatment has been proven effective[1,3,6]. "
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