2008
DOI: 10.1159/000121471
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Overview of the Pathology of Three Widely Used Animal Models of Acute Lung Injury

Abstract: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are syndromes of acute diffuse damage to the pulmonary parenchyma by a variety of local or systemic insults. Increased alveolar capillary membrane permeability was recognized as the common end organ injury and a central feature in all forms of ALI/ARDS. Although great strides have been made in understanding the pathogenesis of ALI/ARDS and in intensive care medicine, the treatment approach to ARDS is still relying on ventilatory and cardiov… Show more

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Cited by 153 publications
(148 citation statements)
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References 158 publications
(102 reference statements)
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“…The present study investigated the protective effects of PNS on ALI induced in a rat model. ALI was induced using oleic acid (OA) and LPS (23). OA has been reported to inhibit alveolar fluid reabsorption, which is a significant problem in ARDS (24).…”
Section: Introductionmentioning
confidence: 99%
“…The present study investigated the protective effects of PNS on ALI induced in a rat model. ALI was induced using oleic acid (OA) and LPS (23). OA has been reported to inhibit alveolar fluid reabsorption, which is a significant problem in ARDS (24).…”
Section: Introductionmentioning
confidence: 99%
“…Although previous studies have reported a reduction in mortality, due to the implementation of lung-protective ventilation strategies, the mortality rate remains high (~40%) (1,2). One of the main pathogenetic factors is sepsis and certain studies have demonstrated that sepsis-induced ALI/ARDS is closely associated with levels of lipopolysaccharide (LPS) in plasma (3). Systemic inflammatory response syndrome (SIRS) is induced by pro-and anti-inflammatory cytokine imbalance and has a detrimental role in LPS-induced ALI/ARDS.…”
Section: Introductionmentioning
confidence: 99%
“…These injury models were selected because of their ability to induce massive lung inflammation as well as to disrupt endothelial barrier functions (26,27). As shown in Fig.…”
Section: C1q Deficiency Exacerbates Lps and Hcl-induced Lungmentioning
confidence: 99%