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Updated: Jul 4, 2026
A Rat Lung Transplantation Model of Warm Ischemia/Reperfusion Injury: Optimizations to Improve Outcomes
Published on: October 28, 2021
Ulinastatin suppresses systemic inflammatory response following lung ischemia-reperfusion injury in rats
1Department of Thoracic Surgery, Cancer Institute and Hospital of Jiangsu Province, Jiangsu, China.
Objective:
We sought to investigate whether ulinastatin (urinary trypsin inhibitor) inhibited systemic inflammatory responses following lung ischemia-reperfusion (I/R) injury.
Materials And Methods:
Establishing a steady left lung warm I/R model in rats, we randomly divided 32 animals into 4 groups: sham (n = 8); I/R (n = 8); low-dose ulinastatin (5000 U/kg pre-ischemia) + I/R (n = 8); and high-dose ulinastatin (10,000 U/kg pre-ischemia) + I/R (n = 8). Measured variables included plasma concentrations of tumor necrosis factor-alpha (TNF-alpha), as well as interleukin (IL)-6 and IL-8.
Results:
The serum concentrations of TNF-alpha, IL-6, and IL-8 in the ulinastatin pretreated groups were markedly decreased compared with those of the I/R group (P < .05). The levels of TNF-alpha, IL-6, and IL-8 were lower in the high-dose ulinastatin group compared with the low-dose ulinastatin group (P < .05).
Conclusion:
Ulinastatin produced dose-dependent attenuation of the systemic inflammatory response of rats following lung I/R injury.
