THE EFFECTS OF HYPEROXIA EXPOSURE ON LUNG FUNCTION AND PULMONARY SURFACTANT IN A RAT MODEL OF ACUTE LUNG INJURY

2009 ◽  
Vol 35 (5) ◽  
pp. 380-398 ◽  
Author(s):  
Patrick W. Pace ◽  
Li-Juan Yao ◽  
John X. Wilson ◽  
Fred Possmayer ◽  
Ruud A.W. Veldhuizen ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Rat Model ◽  
Pulmonary Surfactant ◽  
Hyperoxia Exposure

High oxygen concentrations predispose mouse lungsto the deleterious effects of high stretch ventilation

2003 ◽  
Vol 94 (3) ◽  
pp. 975-982 ◽  
Author(s):  
Timothy C. Bailey ◽  
Erica L. Martin ◽  
Lin Zhao ◽  
Ruud A. W. Veldhuizen
Keyword(s):  
Mechanical Ventilation ◽  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Inflammatory Cytokines ◽  
Pulmonary Surfactant ◽  
Ex Vivo ◽  
Lung Stretch ◽  
Isolated Lungs ◽  
Mechanical Ventilation Group

Mechanical ventilation is a necessary intervention for patients with acute lung injury. However, mechanical ventilation can propagate acute lung injury and increase systemic inflammation. The exposure to >21% oxygen is often associated with mechanical ventilation yet has not been examined within the context of lung stretch. We hypothesized that mice exposed to >90% oxygen will be more susceptible to the deleterious effects of high stretch mechanical ventilation. C57B1/6 mice were randomized into 48-h exposure of 21 or >90% oxygen; mice were then killed, and isolated lungs were randomized into a nonstretch or an ex vivo, high-stretch mechanical ventilation group. Lungs were assessed for compliance and lavaged for surfactant analysis, and cytokine measurements or lungs were homogenized for surfactant-associated protein analysis. Mice exposed to >90% oxygen + stretch had significantly lower compliance, altered pulmonary surfactant, and increased inflammatory cytokines compared with all other groups. Our conclusion is that 48 h of >90% oxygen and high-stretch mechanical ventilation deleteriously affect lung function to a greater degree than stretch alone.

Surfactant and corticosteroid effects on lung function in a rat model of acute lung injury

2001 ◽  
Vol 29 (11) ◽  
pp. 2169-2175 ◽  
Author(s):  
Chung-Ming Chen ◽  
Chia-Lang Fang ◽  
Chien-Hsi Chang
Keyword(s):  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Rat Model

scholarly journals Effect of different doses of dexmedetomidine on lung function and tissue cell apoptosis in a rat model of hyperoxic acute lung injury

2020 ◽  
Vol 19 (5) ◽  
pp. 1093-1098
Author(s):  
Yan Yang ◽  
Xian Qin ◽  
Chuangang Han ◽  
Yan Huang ◽  
Lei Jin ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Tissue Cell ◽  
High Dose ◽  
Apoptosis Index ◽  
Tnf Α ◽  
Different Doses

Purpose: To study the effect of different doses of dexmedetomidine on lung function and lung tissue cell apoptosis in a rat model of hyperoxic acute lung injury. Methods: Five groups of healthy male Sprague-Dawley rats were used: normal rats, untreated hyperoxic rats, and hyperoxic rats given 3 different doses of dexmedetomidine, with 20 rats in each group. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined usingenzyme-linked immunosorbent assay (ELISA). Parietal paraffin cuts were taken from the right upper lobe for measurement of apoptosis using in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and the apoptosis index was calculated. Results: At 24 and 48 h, the levels of IL-6 and TNF-α in the hyperoxia model group were significantly higher than those in the normal control group, and their levels in the middle- and high-dose groups were markedly lowered, relative to untreated hyperoxia rats (p < 0.05). Apoptosis index in the hyperoxia model rats significantly increased, relative to normal rats (p < 0.05). The apoptosis index in the mediumand high-dose groups decreased significantly (p < 0.05). Conclusion: Dexmedetomidine inhibits inflammatory responses caused by high concentration of oxygen inhalation, minimizes lung injury, improves lung function and inhibits lung apoptosis. Keywords: Dexmedetomidine, Hyperoxia, Acute lung injury, Lung function, Apoptosis

Ulinastatin is a novel candidate drug for sepsis and secondary acute lung injury, evidence from an optimized CLP rat model

2013 ◽  
Vol 17 (3) ◽  
pp. 799-807 ◽  
Author(s):  
Ning Wang ◽  
Xin Liu ◽  
Xinchuan Zheng ◽  
Hongwei Cao ◽  
Guo Wei ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Candidate Drug

The differential expression of novel circular RNAs in an acute lung injury rat model caused by smoke inhalation

2017 ◽  
Vol 74 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Zhiqiang Ye ◽  
Xuhui Liu ◽  
Yuewu Yang ◽  
Xianling Zhang ◽  
Ting Yu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Differential Expression ◽  
Rat Model ◽  
Smoke Inhalation ◽  
Circular Rnas

scholarly journals Corrigendum to: Acute Lung Injury in A Rat Model Of Intestinal Ischemia-Reperfusion: The Potential Time Depended Role Of Phospholipases

2021 ◽  
Vol 263 ◽  
pp. 291
Author(s):  
Georgia Kostopanagiotou ◽  
Efthimios Avgerinos ◽  
Konstantinos Kostopanagiotou ◽  
Nikolaos Arkadopoulos ◽  
Ioanna Andreadou ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Effects of Antibiotic Therapy on Pseudomonas aeruginosa-Induced Lung Injury in a Rat Model

1999 ◽  
Vol 43 (10) ◽  
pp. 2389-2394 ◽  
Author(s):  
Erika J. Ernst ◽  
Satoru Hashimoto ◽  
Joseph Guglielmo ◽  
Teiji Sawa ◽  
Jean-Francois Pittet ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
In Vivo Model ◽  
Antibiotic Administration ◽  
Lung Water ◽  
Alveolar Epithelial ◽  
The Right

ABSTRACT The effect of antibiotics on the acute lung injury induced by virulent Pseudomonas aeruginosa PA103 was quantitatively analyzed in a rat model. Lung injury was induced by the instillation of PA103 directly into the right lower lobes of the lungs of anesthetized rats. The alveolar epithelial injury, extravascular lung water, and total plasma equivalents were measured as separate, independent parameters of acute lung injury. Four hours after the instillation of PA103, all the parameters were increased linearly depending on the dose of P. aeruginosa. Next, we examined the effects of intravenously administered antibiotics on the parameters of acute lung injury in d-galactosamine-sensitized rats. One hour after the rats received 107 CFU of PA103, an intravenous bolus injection of aztreonam (60 mg/kg) or imipenem-cilastatin (30 mg/kg) was administered. Despite an MIC indicating resistance, imipenem-cilastatin improved all the measurements of lung injury; in contrast, aztreonam, which had an MIC indicating sensitivity, did not improve any of the lung injury parameters. The antibiotics did not generate different quantities of plasma endotoxin; therefore, endotoxin did not appear to explain the differences in lung injury. This in vivo model is useful to quantitatively compare the efficacies of parenteral antibiotic administration on Pseudomonas airspace infections.

S-nitroso human serum albumin given after LPS challenge reduces acute lung injury and prolongs survival in a rat model of endotoxemia

2008 ◽  
Vol 379 (3) ◽  
pp. 281-290 ◽  
Author(s):  
A. Jakubowski ◽  
N. Maksimovich ◽  
R. Olszanecki ◽  
A. Gebska ◽  
H. Gasser ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Human Serum Albumin ◽  
Lung Injury ◽  
Serum Albumin ◽  
Human Serum ◽  
Rat Model ◽  
Lps Challenge

scholarly journals Adrenomedullin expression in a rat model of acute lung injury induced by hypoxia and LPS

2005 ◽  
Vol 288 (3) ◽  
pp. L536-L545 ◽  
Author(s):  
Jackeline Agorreta ◽  
Javier J. Zulueta ◽  
Luis M. Montuenga ◽  
Mercedes Garayoa
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Lines ◽  
Rat Model ◽  
In Vitro Model ◽  
Rat Lung ◽  
Vitro Model

Adrenomedullin (ADM) is upregulated independently by hypoxia and LPS, two key factors in the pathogenesis of acute lung injury (ALI). This study evaluates the expression of ADM in ALI using experimental models combining both stimuli: an in vivo model of rats treated with LPS and acute normobaric hypoxia (9% O2) and an in vitro model of rat lung cell lines cultured with LPS and exposed to hypoxia (1% O2). ADM expression was analyzed by in situ hybridization, Northern blot, Western blot, and RIA analyses. In the rat lung, combination of hypoxia and LPS treatments overcomes ADM induction occurring after each treatment alone. With in situ techniques, the synergistic effect of both stimuli mainly correlates with ADM expression in inflammatory cells within blood vessels and, to a lesser extent, to cells in the lung parenchyma and bronchiolar epithelial cells. In the in vitro model, hypoxia and hypoxia + LPS treatments caused a similar strong induction of ADM expression and secretion in epithelial and endothelial cell lines. In alveolar macrophages, however, LPS-induced ADM expression and secretion were further increased by the concomitant exposure to hypoxia, thus paralleling the in vivo response. In conclusion, ADM expression is highly induced in a variety of key lung cell types in this rat model of ALI by combination of hypoxia and LPS, suggesting an essential role for this mediator in this syndrome.

scholarly journals Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of neutrophils

2020 ◽  
Author(s):  
Hongxia Mei ◽  
Ying Tao ◽  
Tianhao Zhang ◽  
Feng Qi
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Rat Model ◽  
Neutrophil Function ◽  
Life Threatening ◽  
Pulmonary Inflammatory Response ◽  
Anti Inflammatory ◽  
Factor Α ◽  
The Impact

Abstract Background: Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of neutrophils that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the neutrophil function in a rat model of lipopolysaccharide (LPS)-induced ALI.Results: Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with neutrophil deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced neutrophils via the up-regulation of the ability of neutrophils to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the neutrophil respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated neutrophils, alleviating the damage of neutrophils to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of neutrophils. Conclusion: Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of neutrophils. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.

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