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Pancreatitis-associated pulmonary injury - effects of Lexipafant, a PAF-antagonist

Haraldsen, Pernille; Wang, Xiangdong LU ; Sun, Zhengwu LU ; Börjesson, Anna LU ; Lasson, Åke LU ; Wallén, Rita LU and Andersson, Roland LU (2006) In Journal of Organ Dysfuntion 2(1). p.53-64
Abstract
Objective. Pulmonary injury is an important determinant of outcome in severe acute pancreatitis. The aim of this experimental study was to investigate the potential effect of lexipafant, a platelet-activating factor (PAF) antagonist, on pancreatitis-associated pulmonary injury in experimental acute pancreatitis. Material and methods. Acute pancreatitis was induced by intraductal infusion of 5% sodium taurodeoxycholate in rats that were given the PAF antagonist lexipafant either before (pretreatment) or after (treatment) induction of pancreatitis. Pulmonary endothelial barrier permeability, oedema, protease inhibitor levels, pulmonary ultrastructure and membrane system integrity and levels of interleukin-1 and -6 were evaluated. Results.... (More)
Objective. Pulmonary injury is an important determinant of outcome in severe acute pancreatitis. The aim of this experimental study was to investigate the potential effect of lexipafant, a platelet-activating factor (PAF) antagonist, on pancreatitis-associated pulmonary injury in experimental acute pancreatitis. Material and methods. Acute pancreatitis was induced by intraductal infusion of 5% sodium taurodeoxycholate in rats that were given the PAF antagonist lexipafant either before (pretreatment) or after (treatment) induction of pancreatitis. Pulmonary endothelial barrier permeability, oedema, protease inhibitor levels, pulmonary ultrastructure and membrane system integrity and levels of interleukin-1 and -6 were evaluated. Results. Pulmonary injury was characterized by increased pulmonary endothelial barrier permeability, alveolar oedema and hypoxaemia, which were noted 12 h after the induction of pancreatitis. Pretreatment with lexipafant counteracted the increase in endothelial permeability and partially prevented derangements of protease inhibitor levels. Treatment with lexipafant reduced the severity of pulmonary endothelial barrier dysfunction and diminished the pancreatitis-induced increase in cytokines. Conclusions. PAF seems to play a major role in experimental pancreatitis-associated pulmonary injury and protease inhibitor imbalance. Treatment with a PAF inhibitor may ameliorate pancreatitis-associated pulmonary injury. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Antiproteases, endothelium, interleukins, pancreatitis, permeability, platelet-activating factor, pulmonary injury
in
Journal of Organ Dysfuntion
volume
2
issue
1
pages
53 - 64
publisher
Informa Healthcare
external identifiers
  • scopus:33745090806
ISSN
1747-1060
DOI
10.1080/17471060500424021
language
English
LU publication?
yes
id
7806c520-5199-42af-a379-83e989f14a71 (old id 1137106)
date added to LUP
2008-06-03 14:05:55
date last changed
2019-01-06 06:44:23
@article{7806c520-5199-42af-a379-83e989f14a71,
  abstract     = {Objective. Pulmonary injury is an important determinant of outcome in severe acute pancreatitis. The aim of this experimental study was to investigate the potential effect of lexipafant, a platelet-activating factor (PAF) antagonist, on pancreatitis-associated pulmonary injury in experimental acute pancreatitis. Material and methods. Acute pancreatitis was induced by intraductal infusion of 5% sodium taurodeoxycholate in rats that were given the PAF antagonist lexipafant either before (pretreatment) or after (treatment) induction of pancreatitis. Pulmonary endothelial barrier permeability, oedema, protease inhibitor levels, pulmonary ultrastructure and membrane system integrity and levels of interleukin-1 and -6 were evaluated. Results. Pulmonary injury was characterized by increased pulmonary endothelial barrier permeability, alveolar oedema and hypoxaemia, which were noted 12 h after the induction of pancreatitis. Pretreatment with lexipafant counteracted the increase in endothelial permeability and partially prevented derangements of protease inhibitor levels. Treatment with lexipafant reduced the severity of pulmonary endothelial barrier dysfunction and diminished the pancreatitis-induced increase in cytokines. Conclusions. PAF seems to play a major role in experimental pancreatitis-associated pulmonary injury and protease inhibitor imbalance. Treatment with a PAF inhibitor may ameliorate pancreatitis-associated pulmonary injury.},
  author       = {Haraldsen, Pernille and Wang, Xiangdong and Sun, Zhengwu and Börjesson, Anna and Lasson, Åke and Wallén, Rita and Andersson, Roland},
  issn         = {1747-1060},
  keyword      = {Antiproteases,endothelium,interleukins,pancreatitis,permeability,platelet-activating factor,pulmonary injury},
  language     = {eng},
  number       = {1},
  pages        = {53--64},
  publisher    = {Informa Healthcare},
  series       = {Journal of Organ Dysfuntion},
  title        = {Pancreatitis-associated pulmonary injury - effects of Lexipafant, a PAF-antagonist},
  url          = {http://dx.doi.org/10.1080/17471060500424021},
  volume       = {2},
  year         = {2006},
}