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Updated: Jun 25, 2026

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
Published on: February 26, 2017
Pathogenesis of acute lung injury in rats with severe acute pancreatitis
Xue-Min Liu1, Jun Xu, Zi-Fa Wang
1Department of Hepatobiliary Surgery, First Hospital, Xi'an Jiaotong University, Xi'an 710061, China. a1090224@pub.xaonline.com
Background:
Acute lung injury (ALI) is the most common and severe complication of severe acute pancreatitis (SAP). The elucidation of the mechanism of ALI contributes to the diagnosis and treatment of the illness. In this study, we studied the pathogenesis of ALI in rats with severe acute pancreatitis.
Methods:
The rats were sacrificed at 1, 3, 5, 6, 9 and 12 hours after the establishment of the model of SAP. Pancreas and lung tissues were obtained for pathological study, and examination of microvascular permeability and myeloperoxidase (MPO) examination. The gene expressions of tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas and lung tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR).
Results:
After the establishment of the SAP model, the degree of pancreatic and lung injury increased gradually along with the gradual increase of MPO activity and microvascular permeability. Gene expressions of TNF-alpha and ICAM-1 in the pancreas rose at 1 hour and peaked at 7 hours. In contrast, their gene expression in the lungs rose slightly at 1 hour and peaked at 9-12 hours.
Conclusion:
An obvious time window existed between SAP and lung injury, which is beneficial to the early prevention of the development of ALI.
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Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
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Chronic Pancreatitis I: Introduction
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Acute Pancreatitis I: Introduction
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Chronic Pancreatitis II: Pathophysiology

