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Mast cells contribute to early pancreatitis-induced systemic endothelial barrier dysfunction.

Dib, Marwan LU ; Zhao, Xia LU ; Wang, X and Andersson, Roland LU (2002) In Pancreatology 2(4). p.396-401
Abstract
Background: Activated mast cells can produce and release a number of inflammatory mediators involved in the pathophysiological process of acute conditions. The aim of the study was to evaluate the effect of mast cell stimulation on the early development of multiple organ dysfunction (MODS) in acute pancreatitis (AP). Methods: AP was induced by the intraductal infusion of 5% sodium taurodeoxycholate in the rat. Tissue endothelial barrier dysfunction (TEBD) was measured by plasma exudation of radiolabeled albumin. Activation of mast cells was estimated by measuring the release of histamine. Mast cell stimulation was achieved with compound 48/80 (C48/80) administered intravenously (i.v.) or intraperitoneally (i.p.) in different doses either... (More)
Background: Activated mast cells can produce and release a number of inflammatory mediators involved in the pathophysiological process of acute conditions. The aim of the study was to evaluate the effect of mast cell stimulation on the early development of multiple organ dysfunction (MODS) in acute pancreatitis (AP). Methods: AP was induced by the intraductal infusion of 5% sodium taurodeoxycholate in the rat. Tissue endothelial barrier dysfunction (TEBD) was measured by plasma exudation of radiolabeled albumin. Activation of mast cells was estimated by measuring the release of histamine. Mast cell stimulation was achieved with compound 48/80 (C48/80) administered intravenously (i.v.) or intraperitoneally (i.p.) in different doses either as pretreatment (30 min prior to induction of AP) or treatment immediately after induction of AP. Results: Administration of C48/80 both i.p. and i.v. demonstrated the same effects. A single pretreatment dose of C48/80 (0.5 mg/kg) significantly reduced AP-induced TEBD in the pancreas and gut. Administration of C48/80 immediately after sham operation or induction of AP resulted in a significant increase in pancreatic and intestinal TEBD (p < 0.05 vs. AP+saline). Plasma levels of histamine increased with increasing doses of C48/80. Conclusion: The results imply that mast cell activation could be involved in the initiation of AP and the early phase of AP-induced MODS. Mechanisms seem to be complex and are still to be elucidated. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pancreatology
volume
2
issue
4
pages
396 - 401
publisher
Karger
external identifiers
  • wos:000177304800006
  • pmid:12138228
  • scopus:0035992004
ISSN
1424-3903
DOI
10.1159/000065087
language
English
LU publication?
yes
id
24d1ec60-d88f-4707-bbe3-001cd8920a13 (old id 109607)
alternative location
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12138228&dopt=Abstract
date added to LUP
2007-07-20 09:45:28
date last changed
2017-08-06 03:35:34
@article{24d1ec60-d88f-4707-bbe3-001cd8920a13,
  abstract     = {Background: Activated mast cells can produce and release a number of inflammatory mediators involved in the pathophysiological process of acute conditions. The aim of the study was to evaluate the effect of mast cell stimulation on the early development of multiple organ dysfunction (MODS) in acute pancreatitis (AP). Methods: AP was induced by the intraductal infusion of 5% sodium taurodeoxycholate in the rat. Tissue endothelial barrier dysfunction (TEBD) was measured by plasma exudation of radiolabeled albumin. Activation of mast cells was estimated by measuring the release of histamine. Mast cell stimulation was achieved with compound 48/80 (C48/80) administered intravenously (i.v.) or intraperitoneally (i.p.) in different doses either as pretreatment (30 min prior to induction of AP) or treatment immediately after induction of AP. Results: Administration of C48/80 both i.p. and i.v. demonstrated the same effects. A single pretreatment dose of C48/80 (0.5 mg/kg) significantly reduced AP-induced TEBD in the pancreas and gut. Administration of C48/80 immediately after sham operation or induction of AP resulted in a significant increase in pancreatic and intestinal TEBD (p &lt; 0.05 vs. AP+saline). Plasma levels of histamine increased with increasing doses of C48/80. Conclusion: The results imply that mast cell activation could be involved in the initiation of AP and the early phase of AP-induced MODS. Mechanisms seem to be complex and are still to be elucidated.},
  author       = {Dib, Marwan and Zhao, Xia and Wang, X and Andersson, Roland},
  issn         = {1424-3903},
  language     = {eng},
  number       = {4},
  pages        = {396--401},
  publisher    = {Karger},
  series       = {Pancreatology},
  title        = {Mast cells contribute to early pancreatitis-induced systemic endothelial barrier dysfunction.},
  url          = {http://dx.doi.org/10.1159/000065087},
  volume       = {2},
  year         = {2002},
}