ArticleBurns : journal of the International Society for Burn Injuries2012
Pulmonary microvascular hyperpermeability and expression of vascular endothelial growth factor in smoke inhalation- and pneumonia-induced acute lung injury.
Article in Burns : journal of the International Society for Burn Injuries, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Associated effects of lipopolysaccharide, oleic acid, and lung injury ventilator-induced in developing a model of moderate acute respiratory distress syndrome in New Zealand white rabbits.Frontiers in veterinary science · 2025Article
- Pirfenidone alleviates smoke inhalation lung injury of rats via the NF-κB signaling pathway.Immunity, inflammation and disease · 2024Article
- Comparative proteomic profiling of the ovine and human PBMC inflammatory response.Scientific reports · 2024Article
- Expression of Angiopoietin-2 in Lung Tissue of Juvenile SD Rats with Lipopolysaccharide-Induced Acute Lung Injury and the Role of Ulinastatin.Archivum immunologiae et therapiae experimentalis · 2023Article
- Blocking CXCL1-dependent neutrophil recruitment prevents immune damage and reduces pulmonary bacterial infection after inhalation injury.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Anti-Vascular Endothelial Growth Factor Antibody Suppresses ERK and NF-κB Activation in Ischemia-Reperfusion Lung Injury.PloS one · 2016Article
- Comparison of Gene Expression by Sheep and Human Blood Stimulated with the TLR4 Agonists Lipopolysaccharide and Monophosphoryl Lipid A.PloS one · 2015Article
- Human mesenchymal stem cells reduce the severity of acute lung injury in a sheep model of bacterial pneumonia.Thorax · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionAcute lung injury (ALI) and sepsis are major contributors to the morbidity and mortality of critically ill patients. The current study was designed further evaluate the mechanism of pulmonary vascular hyperpermeability in sheep with these injuries.
methodsSheep were randomized to a sham-injured control group (n=6) or ALI/sepsis group (n=7). The sheep in the ALI/sepsis group received inhalation injury followed by instillation of Pseudomonas aeruginosa into the lungs. These groups were monitored for 24 h. Additional sheep (n=16) received the injury and lung tissue was harvested at different time points to measure lung wet/dry weight ratio, vascular endothelial growth factor (VEGF) mRNA and protein expression as well as 3-nitrotyrosine protein expression in lung homogenates.
resultsThe injury induced severe deterioration in pulmonary gas exchange, increases in lung lymph flow and protein content, and lung water content (P<0.01 each). These alterations were associated with elevated lung and plasma nitrite/nitrate concentrations, increased tracheal blood flow, and enhanced VEGF mRNA and protein expression in lung tissue as well as enhanced 3-nitrotyrosine protein expression (P<0.05 each).
conclusionsThis study describes the time course of pulmonary microvascular hyperpermeability in a clinical relevant large animal model and may improve the experimental design of future studies.
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