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...
Main Authors: | , , , , , , , , |
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Format: | Article |
Language: | English |
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Public Library of Science (PLoS)
2011-01-01
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Series: | PLoS ONE |
Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698290/?tool=EBI |
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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 |
collection | DOAJ |
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. |
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id | doaj.art-1c30db448b66402697f4458d015a287a |
institution | Directory Open Access Journal |
issn | 1932-6203 |
language | English |
last_indexed | 2024-12-14T13:10:29Z |
publishDate | 2011-01-01 |
publisher | Public Library of Science (PLoS) |
record_format | Article |
series | PLoS ONE |
spelling | doaj.art-1c30db448b66402697f4458d015a287a2022-12-21T23:00:12ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0166e2055810.1371/journal.pone.0020558Diaphragm muscle weakness in an experimental porcine intensive care unit model.Julien OchalaGuillaume RenaudMonica Llano DiezVaruna C BanduseelaSudhakar AareKarsten AhlbeckPeter J RadellLars I ErikssonLars LarssonIn 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.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698290/?tool=EBI |
spellingShingle | 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. PLoS ONE |
title | 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_short | Diaphragm muscle weakness in an experimental porcine intensive care unit model. |
title_sort | diaphragm muscle weakness in an experimental porcine intensive care unit model |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698290/?tool=EBI |
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