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Respir Physiol Neurobiol. 2015 Jul;212-214:25-32. doi: 10.1016/j.resp.2015.04.003. Epub 2015 Apr 9.

Effects of lipopolysaccharide-induced inflammation on initial lung fibrosis during open-lung mechanical ventilation in rats.

Author information

1
Department of Anaesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer Ufer 1-3, 68165 Mannheim, Germany. Electronic address: Joerg.Krebs@gmx.de.
2
Department of Anaesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer Ufer 1-3, 68165 Mannheim, Germany. Electronic address: Alexander.Kolz@medma.uni-heidelberg.de.
3
Department of Anaesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer Ufer 1-3, 68165 Mannheim, Germany. Electronic address: Charalambos.Tsagogiorgas@umm.de.
4
Department of Surgical Sciences and Integrated Diagnostics, IRCCS AOU San Martino - IST, University of Genoa, Genoa, Italy. Electronic address: ppelosi@hotmail.com.
5
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, 21941-902 Rio de Janeiro, RJ, Brazil. Electronic address: prmrocco@biof.ufrj.br.
6
Department of Anaesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer Ufer 1-3, 68165 Mannheim, Germany. Electronic address: Thomas.Luecke@umm.de.

Abstract

This study aimed to assess the impact of pulmonary inflammation on early fibrotic response in rats challenged with increasing doses of lipopolysaccharide (LPS). Twenty-four rats were randomized and infused with three different increasing doses of continuous LPS infusion (n=8/group) while being ventilated with low tidal volumes and open-lung positive end-expiratory pressure. Another eight animals served as uninjured control group. Hemodynamics, gas exchange, respiratory system mechanics, lung histology, α-smooth muscle actin, plasma cytokines, and mRNA expression of cytokines and type I and III procollagen in lung tissue were assessed. We found impaired hemodynamics and gas exchange as well as higher histological lung injury scores and α-smooth muscle actin expressions in the medium LPS dose compared to control and the lower LPS dose. The highest LPS dose did not cause further aggravation of these findings. In all LPS groups type I and III procollagen decreased compared to controls and there was a negative correlation between type III procollagen-RNA expression and proinflammatory mediators.

KEYWORDS:

Acute lung injury; Inflammation; Lipopolysaccharide; Lung fibrosis; Open lung ventilation; α-Smooth muscle actin

PMID:
25864801
DOI:
10.1016/j.resp.2015.04.003
[Indexed for MEDLINE]

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