Document Detail

Graded experimental acute pancreatitis: monitoring of a renewed rabbit model focusing on the production of interleukin-8 (IL-8) and CD11b/CD18.
MedLine Citation:
PMID:  10102224     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To establish and monitor a rabbit model of graded severity of acute pancreatitis to test the hypothesis that interleukin-8 (IL-8) and the adhesion molecule complex CD11b/CD18 are involved in the development of systemic complications in severe acute pancreatitis. METHODS: Acute pancreatitis induction in rabbits by duct ligation with or without infusion of 5.0% or 0.5% chenodeoxycholic acid or 0.9% saline. Control animals underwent laparotomy. The animals were monitored biochemically, histologically and immunohistochemically. RESULT: Increased serum levels of IL-8, tumour necrosis factor alpha (TNF-alpha), amylase and lipase were found in the chenodeoxycholic acid groups when compared with the saline, duct-ligated or control groups. Leukopenia, hypocalcaemia, and hyperglycaemia were marked in the 5.0% chenodeoxycholic acid group as compared to the saline, duct-ligated and control groups. Histologically, the 5.0% chenodeoxycholic acid group manifested a significant degree of pancreatic necrosis and neutrophil infiltration. The lungs of these animals showed acute lung injury and a significant up-regulation of CD11b/CD18. IL-8 was produced in pancreatic acinar and ductal cells. A significantly large output of ascitic fluid was seen in the 5.0% chenodeoxycholic acid group. CONCLUSION: The rabbit models of acute pancreatitis are reliable in that enzymatic and histological evidence of acute pancreatitis with or without systemic complications developed. IL-8 is produced locally in pancreatic acinar and ductal cells and significantly increased in peripheral blood during severe but not mild pancreatitis. The expression of the adhesion molecule complex CD11b/CB18 is significantly increased in lung tissue during severe acute pancreatitis with acute lung injury. IL-8 and CD11b/CB18 are involved in the pathogenesis of severe acute pancreatitis but not of mild oedematous pancreatitis.
M O Osman; S B Lausten; N O Jakobsen; J U Kristensen; B Deleuran; C G Larsen; S L Jensen
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of gastroenterology & hepatology     Volume:  11     ISSN:  0954-691X     ISO Abbreviation:  Eur J Gastroenterol Hepatol     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-05-17     Completed Date:  1999-05-17     Revised Date:  2009-10-16    
Medline Journal Info:
Nlm Unique ID:  9000874     Medline TA:  Eur J Gastroenterol Hepatol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  137-49     Citation Subset:  IM    
Department of Surgery, Arhus University Hospital, Denmark.
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MeSH Terms
Acute Disease
Amylases / blood
Antigens, CD11 / biosynthesis*
Antigens, CD18 / biosynthesis*
Ascites / metabolism
Chenodeoxycholic Acid / adverse effects
Cholagogues and Choleretics / adverse effects
Disease Models, Animal
Hyperglycemia / etiology
Hypocalcemia / etiology
Interleukin-8 / biosynthesis*,  blood
Leukopenia / etiology
Lipase / blood
Neutrophils / pathology
Pancreas / pathology
Pancreatic Ducts / surgery
Pancreatitis / blood,  etiology,  immunology*,  pathology
Respiratory Distress Syndrome, Adult / etiology,  immunology
Sodium Chloride
Tumor Necrosis Factor-alpha / analysis
Reg. No./Substance:
0/Antigens, CD11; 0/Antigens, CD18; 0/Cholagogues and Choleretics; 0/Interleukin-8; 0/Tumor Necrosis Factor-alpha; 474-25-9/Chenodeoxycholic Acid; 7647-14-5/Sodium Chloride; EC; EC 3.2.1.-/Amylases
Comment In:
Eur J Gastroenterol Hepatol. 1999 Feb;11(2):125-7   [PMID:  10102222 ]

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