Diaphragm muscle weakness in an experimental porcine intensive care unit model.

In critically ill patients, mechanisms underlying diaphragm muscle remodeling and resultant dysfunction contributing to weaning failure remain unclear. Ventilator-induced modifications as well as sepsis and administration of pharmacological agents such as corticosteroids and neuromuscular blocking a...

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Autores principales: Julien Ochala, Guillaume Renaud, Monica Llano Diez, Varuna C Banduseela, Sudhakar Aare, Karsten Ahlbeck, Peter J Radell, Lars I Eriksson, Lars Larsson
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Publicado: Public Library of Science (PLoS) 2011
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Acceso en línea:https://doaj.org/article/1c30db448b66402697f4458d015a287a
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spelling oai:doaj.org-article:1c30db448b66402697f4458d015a287a2021-11-18T06:52:00ZDiaphragm muscle weakness in an experimental porcine intensive care unit model.1932-620310.1371/journal.pone.0020558https://doaj.org/article/1c30db448b66402697f4458d015a287a2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698290/?tool=EBIhttps://doaj.org/toc/1932-6203In critically ill patients, mechanisms underlying diaphragm muscle remodeling and resultant dysfunction contributing to weaning failure remain unclear. Ventilator-induced modifications as well as sepsis and administration of pharmacological agents such as corticosteroids and neuromuscular blocking agents may be involved. Thus, the objective of the present study was to examine how sepsis, systemic corticosteroid treatment (CS) and neuromuscular blocking agent administration (NMBA) aggravate ventilator-related diaphragm cell and molecular dysfunction in the intensive care unit. Piglets were exposed to different combinations of mechanical ventilation and sedation, endotoxin-induced sepsis, CS and NMBA for five days and compared with sham-operated control animals. On day 5, diaphragm muscle fibre structure (myosin heavy chain isoform proportion, cross-sectional area and contractile protein content) did not differ from controls in any of the mechanically ventilated animals. However, a decrease in single fibre maximal force normalized to cross-sectional area (specific force) was observed in all experimental piglets. Therefore, exposure to mechanical ventilation and sedation for five days has a key negative impact on diaphragm contractile function despite a preservation of muscle structure. Post-translational modifications of contractile proteins are forwarded as one probable underlying mechanism. Unexpectedly, sepsis, CS or NMBA have no significant additive effects, suggesting that mechanical ventilation and sedation are the triggering factors leading to diaphragm weakness in the intensive care unit.Julien OchalaGuillaume RenaudMonica Llano DiezVaruna C BanduseelaSudhakar AareKarsten AhlbeckPeter J RadellLars I ErikssonLars LarssonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 6, p e20558 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Julien Ochala
Guillaume Renaud
Monica Llano Diez
Varuna C Banduseela
Sudhakar Aare
Karsten Ahlbeck
Peter J Radell
Lars I Eriksson
Lars Larsson
Diaphragm muscle weakness in an experimental porcine intensive care unit model.
description In critically ill patients, mechanisms underlying diaphragm muscle remodeling and resultant dysfunction contributing to weaning failure remain unclear. Ventilator-induced modifications as well as sepsis and administration of pharmacological agents such as corticosteroids and neuromuscular blocking agents may be involved. Thus, the objective of the present study was to examine how sepsis, systemic corticosteroid treatment (CS) and neuromuscular blocking agent administration (NMBA) aggravate ventilator-related diaphragm cell and molecular dysfunction in the intensive care unit. Piglets were exposed to different combinations of mechanical ventilation and sedation, endotoxin-induced sepsis, CS and NMBA for five days and compared with sham-operated control animals. On day 5, diaphragm muscle fibre structure (myosin heavy chain isoform proportion, cross-sectional area and contractile protein content) did not differ from controls in any of the mechanically ventilated animals. However, a decrease in single fibre maximal force normalized to cross-sectional area (specific force) was observed in all experimental piglets. Therefore, exposure to mechanical ventilation and sedation for five days has a key negative impact on diaphragm contractile function despite a preservation of muscle structure. Post-translational modifications of contractile proteins are forwarded as one probable underlying mechanism. Unexpectedly, sepsis, CS or NMBA have no significant additive effects, suggesting that mechanical ventilation and sedation are the triggering factors leading to diaphragm weakness in the intensive care unit.
format article
author Julien Ochala
Guillaume Renaud
Monica Llano Diez
Varuna C Banduseela
Sudhakar Aare
Karsten Ahlbeck
Peter J Radell
Lars I Eriksson
Lars Larsson
author_facet Julien Ochala
Guillaume Renaud
Monica Llano Diez
Varuna C Banduseela
Sudhakar Aare
Karsten Ahlbeck
Peter J Radell
Lars I Eriksson
Lars Larsson
author_sort Julien Ochala
title Diaphragm muscle weakness in an experimental porcine intensive care unit model.
title_short Diaphragm muscle weakness in an experimental porcine intensive care unit model.
title_full Diaphragm muscle weakness in an experimental porcine intensive care unit model.
title_fullStr Diaphragm muscle weakness in an experimental porcine intensive care unit model.
title_full_unstemmed Diaphragm muscle weakness in an experimental porcine intensive care unit model.
title_sort diaphragm muscle weakness in an experimental porcine intensive care unit model.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/1c30db448b66402697f4458d015a287a
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