The involvement of multiple protease-antiprotease systems and gut origin sepsis in zymosan-associated endothelial barrier injury and multiple organ dysfunction in rats
(2001) In Shock 16(4). p.298-303- Abstract
- Multiple organ dysfunction syndrome is a dominant cause of mortality in the intensive care unit. Experimentally, a condition similar to the multiple organ dysfunction syndrome can be induced by the intraperitoneal injection of sterile zymosan. In the present study we investigate potential alterations in multiple organ functions, endothelial permeability, and antiproteinases after intraperitoneal injection of zymosan at various doses. Zymosan-induced generalized inflammation lead to endothelial barrier injury in multiple organs/tissues, a decrease in systemic arterial pressure, impaired organ function and gut defence function, and consumption of protease inhibitors, particularly the consumption of alpha (2) antiplasmin. Endothelial barrier... (More)
- Multiple organ dysfunction syndrome is a dominant cause of mortality in the intensive care unit. Experimentally, a condition similar to the multiple organ dysfunction syndrome can be induced by the intraperitoneal injection of sterile zymosan. In the present study we investigate potential alterations in multiple organ functions, endothelial permeability, and antiproteinases after intraperitoneal injection of zymosan at various doses. Zymosan-induced generalized inflammation lead to endothelial barrier injury in multiple organs/tissues, a decrease in systemic arterial pressure, impaired organ function and gut defence function, and consumption of protease inhibitors, particularly the consumption of alpha (2) antiplasmin. Endothelial barrier injury appears to present a dose- and organ-dependent pattern in multiple organs/tissues, and the increase in endothelial barrier permeability occurred prior to organ dysfunction. Zymosan induced the development of multiple organ dysfunction syndrome, probably initiating multiple protease-antiprotease systems, particularly the fibrinolytic system, leading to endothelial barrier injury, tissue edema, parenchymal cell damage, and eventual organ dysfunction, potentially augmented by a secondary bacterial infection. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1121831
- author
- Deng, XM ; Wang, XD ; Lasson, Åke LU ; Sun, ZW ; Soltesz, Vasile LU and Andersson, Roland LU
- organization
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Shock
- volume
- 16
- issue
- 4
- pages
- 298 - 303
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- wos:000170970300012
- scopus:0035490816
- ISSN
- 1540-0514
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Surgery (Lund) (013009000), Division of Medical Microbiology (013250400), Emergency medicine/Medicine/Surgery (013240200)
- id
- dcdf704c-7d19-4f23-b03e-f51010e1ebfc (old id 1121831)
- date added to LUP
- 2016-04-01 11:41:02
- date last changed
- 2022-01-26 08:39:23
@article{dcdf704c-7d19-4f23-b03e-f51010e1ebfc,
abstract = {{Multiple organ dysfunction syndrome is a dominant cause of mortality in the intensive care unit. Experimentally, a condition similar to the multiple organ dysfunction syndrome can be induced by the intraperitoneal injection of sterile zymosan. In the present study we investigate potential alterations in multiple organ functions, endothelial permeability, and antiproteinases after intraperitoneal injection of zymosan at various doses. Zymosan-induced generalized inflammation lead to endothelial barrier injury in multiple organs/tissues, a decrease in systemic arterial pressure, impaired organ function and gut defence function, and consumption of protease inhibitors, particularly the consumption of alpha (2) antiplasmin. Endothelial barrier injury appears to present a dose- and organ-dependent pattern in multiple organs/tissues, and the increase in endothelial barrier permeability occurred prior to organ dysfunction. Zymosan induced the development of multiple organ dysfunction syndrome, probably initiating multiple protease-antiprotease systems, particularly the fibrinolytic system, leading to endothelial barrier injury, tissue edema, parenchymal cell damage, and eventual organ dysfunction, potentially augmented by a secondary bacterial infection.}},
author = {{Deng, XM and Wang, XD and Lasson, Åke and Sun, ZW and Soltesz, Vasile and Andersson, Roland}},
issn = {{1540-0514}},
language = {{eng}},
number = {{4}},
pages = {{298--303}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Shock}},
title = {{The involvement of multiple protease-antiprotease systems and gut origin sepsis in zymosan-associated endothelial barrier injury and multiple organ dysfunction in rats}},
volume = {{16}},
year = {{2001}},
}