A new model of acute respiratory distress syndrome due to smoke inhalation and cutaneous burns in swine

To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and persisted for 24 h after insult. Conversely, FS disrupted 51.4, 55.6, 46.3, and 43.0% enzymatic activity of neutral endopeptidase (NEP, a primary hydrolyzing enzyme for SP) 1, 6, 12, and 24 h after insult, respectively. Immunolabeling density of NEP in the airway epithelium largely disappeared 1 h after insult due to acute cell damage and shedding. These changes were also accompanied by extensive influx of albumin and granulocytes/lymphocytes in BALF. Furthermore, levels of BALF SP and tissue NEP activity dose dependently increased and decreased, respectively, following 0, low (10 min), and high (20 min) levels of FS inhalation. However, neither the time-course nor the dose-response study observed a significant change in the highest affinity neurokinin-1 receptor (NK-1R) for SP. Finally, treatment (10 mg/kg im) with SR-140333B, an NK-1R antagonist, significantly prevented 20-min FS-induced hypoxemia and pulmonary edema 24 h after insult. Further examination indicated that SR-140333B (1.0 or 10.0 mg/kg im) fully abolished early (1 h) plasma extravasation following FS. Collectively, these findings suggest that a combination of sustained SP and NEP inactivity induces an exaggerated neurogenic inflammation mediated by NK-1R, which may lead to an uncontrolled influx of protein-rich edema fluid and cells into the alveoli as a consequence of increased vascular permeability.

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Use of Nebulized Heparin, Nebulized N-Acetylcysteine, and Nebulized Epoprostenol in a Patient With Smoke Inhalational Injury and Acute Respiratory Distress Syndrome

Journal of Pharmacy Practice ◽

10.1177/0897190016663071 ◽

2016 ◽

Vol 30 (6) ◽

pp. 663-667 ◽

Cited By ~ 4

Author(s):

Kevin M. Dube ◽

Kristen L. Ditch ◽

Luanne Hills

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Concomitant Administration ◽

Smoke Inhalation ◽

Bronchial Obstruction ◽

Smoke Inhalation Injury ◽

First Case ◽

Pulmonary Vasodilator

Smoke inhalation injury (SIJ) is associated with an increase in morbidity and mortality in patients with burns. SIJ causes airway damage, inflammation, and bronchial obstruction, resulting in decreased oxygenation and perfusion status in these patients. Retrospective studies have compared the use of nebulized heparin (NH) plus nebulized N-acetylcysteine (NAC) and albuterol in patients with SIJ to those who received standard ventilator support with bronchodilator therapy. These studies are associated with a decrease in mortality when NH and nebulized NAC are administered to patients with SIJ. Approximately 20% of patients who develop SIJ will also develop acute respiratory distress syndrome (ARDS). Epoprostenol, a selective pulmonary vasodilator, has been utilized in the treatment of ARDS with mixed results for improving gas exchange. To our knowledge, this is the first case report of the concomitant administration of NH, nebulized NAC, and nebulized epoprostenol following SIJ in a burn patient with ARDS.

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Zinc chloride smoke inhalation: a rare cause of severe acute respiratory distress syndrome

Intensive Care Medicine ◽

10.1007/s001340050049 ◽

2000 ◽

Vol 26 (2) ◽

pp. 215-217 ◽

Cited By ~ 26

Author(s):

V. Pettilä ◽

O. Takkunen ◽

P. Tukiainen

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Zinc Chloride ◽

Distress Syndrome ◽

Smoke Inhalation

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The Construction of A Sheep Acute Respiratory Distress Syndrome Model Induced by Smoke Inhalation Injury

Medical Research ◽

10.6913/mrhk.201912_1(1).0001 ◽

2019 ◽

Vol 1 (1) ◽

pp. 1-11

Author(s):

Fei YU ◽

Yuan-fei TAN ◽

Guan-nan SHENG ◽

Guan-nan CHEN ◽

Nan-nan WANG ◽

...

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Lung Injury ◽

Confidence Interval ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Exposure Time ◽

Distress Syndrome ◽

Oxygenation Index ◽

Smoke Exposure ◽

Smoke Inhalation

Objective To establish a model of acute respiratory distress syndrome induced by sheep smoke inhalation lung injury. Methods Nine healthy, 12-24 month old, non-pregnant female sheep were randomly selected, the sheep were divided into three groups, through the internal control of smoke generator device components (CO, CO2, O2, particle concentration and smoke temperature, etc.) to adjust the exposure time of the sheep model construction of smoke. The chest CT were examined before and after exposure to smoke at 6h, 12h, 24h and 48h, respectively. From the smoke exposure 12h endotracheal intubation and mechanical ventilation, by adjusting the ventilator parameters of hypoxemia and hypercapnia, statistical analysis of PaO2/FiO2, PEEP and other indicators, according to the ARDS definition of diagnosis in Berlin definition. Results The CT showed mild inflammation of the lungs in first group, oxygen index of 95% confidence interval [331.13, 353.53]; In second groups, oxygenation index 95% confidence interval [220.09, 383.90]; CT showed airway edema, pulmonary inflammatory exudation and lung injury in third group. Oxygenation index 95% confidence interval of [195.16, 244.84], PEEP>5cm. There was significant difference between the two groups (P<0.05). Conclusions The severity of lung injury can be changed by adjusting the exposure time of smoke inhalation; when the smoke exposure time up to 45 minutes, a stable model of smoke inhalation lung injury in sheep ARDS can be successfully established.

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