Related Experiment Video
Updated: Jul 8, 2026

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
N-acetylcysteine attenuates acute lung injury induced by fat embolism
Demeral David Liu1, Shang-Jhy Kao, Hsing I Chen
1Department of Dentistry and Neuro-Medical Scientific Center, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan.
Objectives:
Fat embolism syndrome is a clinical issue in subjects with long-bone fracture. It may lead to acute lung injury. The mechanisms and therapeutic regimen remain unclear. The present study was designed to investigate the pathologic and biochemical changes after fat embolization in isolated rat lungs, and to test the effects of posttreatment with N-acetylcysteine (NAC).
Design:
Prospective, randomized, controlled animal study.
Setting:
University research laboratory.
Subjects:
A total of 36 perfused lungs isolated from Sprague-Dawley rats.
Interventions:
The isolated lungs were randomly assigned to receive physiologic saline solution (vehicle group), fat embolism (FE group), or FE with NAC posttreatment (FE + NAC group). There were 12 isolated lungs in each group. FE was produced by introduction of corn oil micelles. NAC at a dose 150 mg/kg was given 10 mins after FE.
Measurements And Main Results:
The extent of acute lung injury was evaluated by lung weight change, protein concentration in bronchoalveolar lavage, and exhaled nitric oxide. We also measured the pulmonary arterial pressure and capillary filtration coefficient and determined the nitrate/nitrite, methylguanidine, tumor necrosis factor-alpha, and interleukin-1beta in lung perfusate. Histopathologic changes of the lung were examined and quantified. The levels of neutrophil elastase and myeloperoxidase were determined. The expression of inducible nitric oxide synthase was detected. FE caused acute lung injury as evidenced by the lung weight changes, increases in exhaled nitric oxide and protein concentration in bronchoalveolar lavage, pulmonary hypertension, increased capillary filtration coefficient, and lung pathology. The insult also increased nitrate/nitrite, methylguanidine, tumor necrosis factor-alpha, and interleukin-1beta in lung perfusate, increased neutrophil elastase and myeloperoxidase levels, and upregulated inducible nitric oxide synthase expression. Posttreatment with NAC abrogated these changes induced by FE.
Conclusion:
FE caused acute lung injury and associated biochemical changes. Posttreatment with NAC was effective to alleviate the pathologic and biochemical changes caused by FE.
Related Concept Videos
Acute Respiratory Failure-V
Ensure that patients are monitored continuously for their response to therapy, including changes in...
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care
Acute Pancreatitis II: Pathophysiology
Chronic Obstructive Pulmonary Disease II: Emphysema
Pulmonary Embolism III: Nursing Management
Anticholinesterase Agents: Poisoning and Treatment
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...

