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Updated: Jun 17, 2026

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
Pancreatic injury in rabbits with acute renal failure
Zi-Gang Zhao1, Chun-Yu Niu, Yu-Ping Zhang
1Institute of Microcirculation, Hebei North University, Hebei Zhangjiakou 075029, China.
Background:
Acute renal failure (ARF) is a common critical disorder. To decrease the mortality, it is important to prevent ARF from invading other organs in clinical setting. It is not known whether there is a dysfunction in pancreas during the pathogenesis of ARF. This study aimed to investigate the changes of morphology and function on pancreas in ARF rabbits.
Methods:
Sixty rabbits were randomly divided into four groups. The ARF model of groups 1 and 2 rabbits was established by hypodermic injection of 1% HgCl(2) (1.3 mL/kg) and intramuscular injection of 50% glyceritum (10 mL/kg), respectively. The control groups 1 and 2 were injected with same volume of normal saline. After 24 hours, urea and creatinine contents and pancreatic amylase (AMY) activities in serum were measured using an automatic biochemical analyzer; the insulin levels were measured with radioimmunoassay method. Moreover, morphological alterations were examined by light microscopy; free radicals, nitric oxide (NO), and nitric oxide synthase (NOS) in pancreas homogenate were determined.
Results:
Morphological study showed that there were vacuolar degeneration and necrosis in pancreas of ARF for both groups 1 and 2. Compared with corresponding control group, the AMY activity was significantly elevated, whereas the INS values were decreased significantly in ARF groups 1 and 2. Malonaldehyde, NO, and NOS in pancreas homogenate were significantly increased, and superoxide dismutase activity was decreased.
Conclusion:
These data suggested that there were morphological damage of pancreas and disturbance of pancreatic secretion function in rabbits with ARF. Free radicals-injury and NO excessive release may explain the observed dysfunction.
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