4.5 Article

A novel large animal model of smoke inhalation-induced acute respiratory distress syndrome

期刊

RESPIRATORY RESEARCH
卷 22, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12931-021-01788-8

关键词

Smoke inhalation; ARDS; Large animal model; Toxic inhalation injury; Hypoxia; Hypoxemia

资金

  1. Department of Defense U.S. Air Force [FA4600-12-D-9000]

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This study successfully developed a novel large animal model to simulate smoke inhalation-induced ARDS, which could be beneficial for studying the pathophysiology of inhalation injury or developing new therapeutics.
Background Acute respiratory distress syndrome (ARDS) is multifactorial and can result from sepsis, trauma, or pneumonia, amongst other primary pathologies. It is one of the major causes of death in critically ill patients with a reported mortality rate up to 45%. The present study focuses on the development of a large animal model of smoke inhalation-induced ARDS in an effort to provide the scientific community with a reliable, reproducible large animal model of isolated toxic inhalation injury-induced ARDS. Methods Animals (n = 21) were exposed to smoke under general anesthesia for 1 to 2 h (median smoke exposure = 0.5 to 1 L of oak wood smoke) after the ultrasound-guided placement of carotid, pulmonary, and femoral artery catheters. Peripheral oxygen saturation (SpO(2)), vital signs, and ventilator parameters were monitored throughout the procedure. Chest x-ray, carotid, femoral and pulmonary artery blood samples were collected before, during, and after smoke exposure. Animals were euthanized and lung tissue collected for analysis 48 h after smoke inhalation. Results Animals developed ARDS 48 h after smoke inhalation as reflected by a decrease in SpO(2) by approximately 31%, PaO2/FiO(2) ratio by approximately 208 (50%), and development of bilateral, diffuse infiltrates on chest x-ray. Study animals also demonstrated a significant increase in IL-6 level, lung tissue injury score and wet/dry ratio, as well as changes in other arterial blood gas (ABG) parameters. Conclusions This study reports, for the first time, a novel large animal model of isolated smoke inhalation-induced ARDS without confounding variables such as cutaneous burn injury. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury or for development of novel therapeutics.

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