Comparison of direct and indirect models of early induced acute lung injury

The animal experimental counterpart of human acute respiratory distress syndrome (ARDS) is acute lung injury (ALI). Most models of ALI involve reproducing the clinical risk factors associated with human ARDS, such as sepsis or acid aspiration; however, none of these models fully replicates human ARD...

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Detalles Bibliográficos
Autores: Chimenti, Laura|||0000-0002-3109-7779, Morales-Quinteros, Luis|||0000-0002-8937-9824, Puig, Ferranda, Camprubí-Rimblas, Marta|||0000-0002-4085-5324, Guillamat-Prats, Raquel|||0000-0001-6960-0985, Gómez, Maria Nieves, Tijero, Jessica, Blanch, Lluís|||0000-0002-4158-7464, Matute-Bello, Gustavo, Artigas Raventós, Antoni|||0000-0002-8029-1017
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:238698
Acceso en línea:https://ddd.uab.cat/record/238698
https://dx.doi.org/urn:doi:10.1186/s40635-020-00350-y
Access Level:acceso abierto
Palabra clave:Acute lung injury
Animal models
Hydrochloric acid
Cecal ligation puncture
Lipopolysaccharide
Descripción
Sumario:The animal experimental counterpart of human acute respiratory distress syndrome (ARDS) is acute lung injury (ALI). Most models of ALI involve reproducing the clinical risk factors associated with human ARDS, such as sepsis or acid aspiration; however, none of these models fully replicates human ARDS. To compare different experimental animal models of ALI, based on direct or indirect mechanisms of lung injury, to characterize a model which more closely could reproduce the acute phase of human ARDS. Adult male Sprague-Dawley rats were subjected to intratracheal instillations of (1) HCl to mimic aspiration of gastric contents; (2) lipopolysaccharide (LPS) to mimic bacterial infection; (3) HCl followed by LPS to mimic aspiration of gastric contents with bacterial superinfection; or (4) cecal ligation and puncture (CLP) to induce peritonitis and mimic sepsis. Rats were sacrificed 24 h after instillations or 24 h after CLP. At 24 h, rats instilled with LPS or HCl-LPS had increased lung permeability, alveolar neutrophilic recruitment and inflammatory markers (GRO/KC, TNF-α, MCP-1, IL-1β, IL-6). Rats receiving only HCl or subjected to CLP had no evidence of lung injury. Rat models of ALI induced directly by LPS or HCl-LPS more closely reproduced the acute phase of human ARDS than the CLP model of indirectly induced ALI.