November 12, 2014
Notes: Lei, Huang
Research Support, Non-U.S. Gov’t
Turk J Gastroenterol. 2013;24(6):502-7.
Author Address: Emergency Department, West China Hospital, Sichuan University, Chengdu, Sichuan Province 610041, China.
Reference Type: Journal Article
Record Number: 4707Author: Li, W. D., Jia, L., Ou, Y., Huang, Y. X. and Jiang, S. M.
Title: Surveillance of intra-abdominal pressure and intestinal barrier function in a rat model of acute necrotizing pancreatitis and its potential early therapeutic window
Journal: PLoS One
Short Title: Surveillance of intra-abdominal pressure and intestinal barrier function in a rat model of acute necrotizing pancreatitis and its potential early therapeutic window
Alternate Journal: PloS one
ISSN: 1932-6203 (Electronic)
Accession Number: 24244397
Keywords: Amine Oxidase (Copper-Containing)/blood
Cholagogues and Choleretics/*adverse effects/pharmacology
Disease Models, Animal
*Pancreatitis, Acute Necrotizing/blood/chemically induced/physiopathology/therapy
Taurocholic Acid/*adverse effects/pharmacology
Tumor Necrosis Factor-alpha/blood
Abstract: OBJECTIVES: To monitor intra-abdominal pressure (IAP) and intestinal barrier function in a rat model of acute necrotizing pancreatitis (ANP) to elucidate a potential relevant therapeutic window. METHODS: Sprague-Dawley rats were randomly divided into experimental or control groups. The ANP group (n = 40) was injected with 4.5% sodium taurocholate into the pancreatic duct to induce ANP. The controls received only abdominal opening surgery (sham-operated, SO; n = 40) or no treatment or surgery (baseline; 0 h, n = 20). The SO and ANP groups were then randomly subdivided into 3, 6, 12 and 24 h groups (n = 10 each). IAP was measured at each time point and the rats were sacrificed to measure the weight of accumulated ascites fluid and the amylase, endogenous creatinine (Cr), total bilirubin (TB), tumor necrosis factor- alpha (TNF-alpha), diamine oxidase (DAO), and D-lactate. Mortality and the development of pathological changes in the pancreas and intestines were also monitored. RESULTS: IAP showed a continuous upward trend in the ANP group, with values 2 to 3 times higher than those in the SO group at the corresponding time points and the rising rate was peaking at 6 h. The levels of plasma amylase, TNF-alpha, Cr, TB, DAO, and D-lactate also gradually increased in the ANP group over time and were significantly higher than in the SO group at 3, 6, 12 and 24 h (all P<0.05). Moreover, the rising rate of TNF-alpha, DAO, and D-lactate also peaked at 6 h. CONCLUSIONS: The ANP-induced changes in IAP, inflammatory factors and intestinal barrier that we observed in the rat model were especially obvious at 6 h post-induction, suggesting an early therapeutic window for the treatment of ANP in humans.