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Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model

INTRODUCTION: The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a “lung-brain...

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Autores principales: Kamuf, Jens, Garcia-Bardon, Andreas, Ziebart, Alexander, Thomas, Rainer, Folkert, Konstantin, Frauenknecht, Katrin, Thal, Serge C., Hartmann, Erik K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6084980/
https://www.ncbi.nlm.nih.gov/pubmed/30092082
http://dx.doi.org/10.1371/journal.pone.0202131
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author Kamuf, Jens
Garcia-Bardon, Andreas
Ziebart, Alexander
Thomas, Rainer
Folkert, Konstantin
Frauenknecht, Katrin
Thal, Serge C.
Hartmann, Erik K.
author_facet Kamuf, Jens
Garcia-Bardon, Andreas
Ziebart, Alexander
Thomas, Rainer
Folkert, Konstantin
Frauenknecht, Katrin
Thal, Serge C.
Hartmann, Erik K.
author_sort Kamuf, Jens
collection PubMed
description INTRODUCTION: The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a “lung-brain-crosstalk”. Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. METHODS: After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of oleic acid (n = 8), lung injury by bronchoalveolar lavage in combination with one hour of injurious ventilation (n = 8) or control (n = 6). Brain tissue of four native animals from a different study served as native group. For six hours all animals were ventilated with a tidal volume of 7 ml kg(-1) and a scheme for positive end-expiratory pressure and inspired oxygen fraction, which was adapted from the ARDS network tables. Afterwards the animals were killed and the brains were harvested for histological (number of neurons and microglia) and molecular biologic (TNFalpha, IL-1beta, and IL-6) examinations. RESULTS: There was no difference in the number of neurons or microglia cells between the groups. TNFalpha was significantly higher in all groups compared to native (p < 0.05), IL-6 was only increased in the lavage group compared to native (p < 0.05), IL-1beta showed no difference between the groups. DISCUSSION: With our data we can confirm earlier results, that mechanical ventilation itself seems to trigger cerebral inflammation. This is not aggravated by acute lung injury, at least not within the first 6 hours after onset. Nevertheless, it seems too early to dismiss the idea of lung-injury induced cerebral inflammation, as 6 hours might be just not enough time to see any profound effect.
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spelling pubmed-60849802018-08-18 Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model Kamuf, Jens Garcia-Bardon, Andreas Ziebart, Alexander Thomas, Rainer Folkert, Konstantin Frauenknecht, Katrin Thal, Serge C. Hartmann, Erik K. PLoS One Research Article INTRODUCTION: The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a “lung-brain-crosstalk”. Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. METHODS: After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of oleic acid (n = 8), lung injury by bronchoalveolar lavage in combination with one hour of injurious ventilation (n = 8) or control (n = 6). Brain tissue of four native animals from a different study served as native group. For six hours all animals were ventilated with a tidal volume of 7 ml kg(-1) and a scheme for positive end-expiratory pressure and inspired oxygen fraction, which was adapted from the ARDS network tables. Afterwards the animals were killed and the brains were harvested for histological (number of neurons and microglia) and molecular biologic (TNFalpha, IL-1beta, and IL-6) examinations. RESULTS: There was no difference in the number of neurons or microglia cells between the groups. TNFalpha was significantly higher in all groups compared to native (p < 0.05), IL-6 was only increased in the lavage group compared to native (p < 0.05), IL-1beta showed no difference between the groups. DISCUSSION: With our data we can confirm earlier results, that mechanical ventilation itself seems to trigger cerebral inflammation. This is not aggravated by acute lung injury, at least not within the first 6 hours after onset. Nevertheless, it seems too early to dismiss the idea of lung-injury induced cerebral inflammation, as 6 hours might be just not enough time to see any profound effect. Public Library of Science 2018-08-09 /pmc/articles/PMC6084980/ /pubmed/30092082 http://dx.doi.org/10.1371/journal.pone.0202131 Text en © 2018 Kamuf et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Kamuf, Jens
Garcia-Bardon, Andreas
Ziebart, Alexander
Thomas, Rainer
Folkert, Konstantin
Frauenknecht, Katrin
Thal, Serge C.
Hartmann, Erik K.
Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title_full Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title_fullStr Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title_full_unstemmed Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title_short Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
title_sort lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6084980/
https://www.ncbi.nlm.nih.gov/pubmed/30092082
http://dx.doi.org/10.1371/journal.pone.0202131
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