Establishment and evaluation of a Beagle model of grade III pancreatic trauma

Gao,Hanjing; Song,Qing; Lv,Faqin; Shi,Bin; Wang,Pengfei; Wang,Yiru; Zhang,Yan; Yang,Li; Luo,Yukun; Mei,Xingguo; Tang,Jie

doi:10.3892/etm.2018.6656

Establishment and evaluation of a Beagle model of grade III pancreatic trauma

Authors:
- Hanjing Gao
- Qing Song
- Faqin Lv
- Bin Shi
- Pengfei Wang
- Yiru Wang
- Yan Zhang
- Li Yang
- Yukun Luo
- Xingguo Mei
- Jie Tang
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Affiliations: Department of Ultrasound, Chinese PLA General Hospital, Beijing 100853, P.R. China, Department of Ultrasound, General Hospital of Beijing Military Region, Beijing 100700, P.R. China, Department of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, P.R. China, Department of Ultrasound, 161st Hospital of Chinese PLA, Wuhan, Hubei 430010, P.R. China, Department of Pharmaceutics, Beijing Institute of Pharmacology and Toxicology, Beijing 100039, P.R. China
Published online on: August 24, 2018 https://doi.org/10.3892/etm.2018.6656
Pages: 3452-3458
Copyright: © Gao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Pancreatic trauma (PT) is a severe abdominal injury that is often combined with multiple organ injury. It is a severe disease that is difficult to diagnose and has a high mortality rate, particularly for grade III PT. The pathogenesis, disease progress and complications have not been fully investigated due to the lack of a reliable animal model. To address this, a Beagle model of grade III PT was established in the present study using a procedure involving rupture of the main pancreatic duct. Peripancreatic effusions and the degree of pancreatic damage were examined by routine ultrasound and contrast‑enhanced ultrasound (CEUS). Also, ascites were collected for the examination of amylase and lipase levels, and whole blood samples were collected for the analysis of amylase, lipase, C‑reactive protein (CRP), interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α levels in the serum. Urine samples were also collected for the examination of trypsinogen activation peptide (TAP). In addition, the pancreas was sectioned and stained with hematoxylin and eosin. In comparison with routine ultrasound, CEUS showed a large area of focal trauma, with a depth greater than half of the anteroposterior diameter of the pancreas, with a clear boundary, clear capsular rupture and trauma induced by active bleeding. The volume of ascites peaked at 48 h post‑trauma and decreased thereafter. Amylase and lipase levels in the ascites were elevated at 24 h post‑trauma and significantly decreased at 48 and 72 h post‑trauma (P<0.01). In addition, serum amylase and lipase levels increased to peak levels at 48 h post‑trauma and then decreased (P<0.05), while serum CRP, IL‑6 and TNF‑α levels peaked at 24 h post‑trauma and then decreased (P<0.05). Urinary TAP levels also peaked at 24 h post‑trauma and subsequently decreased (P<0.05). At 72 h post‑trauma, the pancreatic cells were loosely distributed, with damaged acini, hyperchromatic nuclei and severe inflammatory cell invasion. These results indicated that the Beagle model of grade III PT was satisfactorily established, and that CEUS is potentially useful as an auxiliary diagnosis method for PT. This animal model may be useful for studying the pathogenesis, disease progress and complications of PT.

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