Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm

Futier, Emmanuel; Constantin, Jean-Michel; Combaret, Lydie; Mosoni, Laurent; Roszyk, Laurence; Sapin, Vincent; Attaix, Didier; Jung, Boris; Jaber, Samir; Bazin, Jean-Étienne

doi:10.1186/cc7010

Cited by 125 publications

(107 citation statements)

References 60 publications

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“…Only one investigation has explored the influence of partial support MV on rat diaphragm protein synthesis. This study reveals that compared with spontaneous breathing animals, partial support ventilation does not promote a significant decrease in diaphragm protein synthesis in vitro (32). How much ventilator support was provided in this study is unknown and whether or not these results can be replicated in vivo remains unclear and warrants additional work.…”

Section: Mv-induced Decreases In Protein Diaphragmatic Synthesismentioning

confidence: 76%

“…Specifically, Futier et al (32) reported that 18 h of partial support MV did not increase proteolysis in the rat diaphragm. In contrast, Hudson et al demonstrated that 18 h of partial support MV activates the 20S proteasome, calpain, and caspase-3 in the diaphragm (44).…”

Section: Mv-induced Proteolysis In the Diaphragmmentioning

confidence: 99%

“…However, animal studies show that full support MV promotes a rapid decline in protein synthesis in the rat diaphragm (32,99 rapidly within the first 6 h of full support MV and remains depressed during the next 12 h of MV (99). Only one investigation has explored the influence of partial support MV on rat diaphragm protein synthesis.…”

Section: Mv-induced Decreases In Protein Diaphragmatic Synthesismentioning

confidence: 99%

See 2 more Smart Citations

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

143

156

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Powers SK, Wiggs MP, Sollanek KJ, Smuder AJ. Ventilator-induced diaphragm dysfunction: cause and effect. Am J Physiol Regul Integr Comp Physiol 305: R464 -R477, 2013. First published July 10, 2013 doi:10.1152/ajpregu.00231.2013 is used clinically to maintain gas exchange in patients that require assistance in maintaining adequate alveolar ventilation. Common indications for MV include respiratory failure, heart failure, drug overdose, and surgery. Although MV can be a life-saving intervention for patients suffering from respiratory failure, prolonged MV can promote diaphragmatic atrophy and contractile dysfunction, which is referred to as ventilator-induced diaphragm dysfunction (VIDD). This is significant because VIDD is thought to contribute to problems in weaning patients from the ventilator. Extended time on the ventilator increases health care costs and greatly increases patient morbidity and mortality. Research reveals that only 18 -24 h of MV is sufficient to develop VIDD in both laboratory animals and humans. Studies using animal models reveal that MV-induced diaphragmatic atrophy occurs due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, autophagy, and the ubiquitin-proteasome system as key proteases that participate in MV-induced diaphragmatic proteolysis. The challenge for the future is to define the MV-induced signaling pathways that promote the loss of diaphragm protein and depress diaphragm contractility. Indeed, forthcoming studies that delineate the signaling mechanisms responsible for VIDD will provide the knowledge necessary for the development of a pharmacological approach that can prevent VIDD and reduce the incidence of weaning problems. respiratory muscle; atrophy; mechanical ventilation; weaning; muscle wasting MECHANICAL VENTILATION (MV) is used clinically to achieve sufficient pulmonary gas exchange in patients unable to sustain adequate alveolar ventilation on their own. Common indications for MV include respiratory failure due to chronic obstructive pulmonary disease, status asthmaticus, and/or heart failure. In addition, MV is often an essential intervention in patients suffering from acute drug overdose, neuromuscular diseases, sepsis, and during surgery along with postsurgical recovery.The number of patients receiving prolonged MV in the United States exceeds more than 300,000 each year in the intensive care unit (ICU) (20). Although MV can be a lifesaving measure, prolonged MV results in the rapid development of diaphragmatic weakness due to both atrophy and contractile dysfunction. This detrimental impact of prolonged MV on the diaphragm has been termed ventilator-induced diaphragmatic dysfunction (VIDD) and VIDD is predicted to be a major contributor to problems in weaning patients from the ventilator (26, 114). Although previous reports describing the impact of prolonged MV on the diaphragm have appeared in the literature, advances in our understanding of the mechanisms responsible for VIDD h...

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Section: Mv-induced Decreases In Protein Diaphragmatic Synthesismentioning

confidence: 76%

Section: Mv-induced Proteolysis In the Diaphragmmentioning

confidence: 99%

Section: Mv-induced Decreases In Protein Diaphragmatic Synthesismentioning

confidence: 99%

See 1 more Smart Citation

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

143

156

View full text Add to dashboard Cite

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“…Barbiturates and neuromuscular blockers have deleterious effects in skeletal muscle function 29 . When applied on an intermittent manner, nevertheless, they do not contribute to VIDD 28 .…”

Section: Analysis Of Experimental Designmentioning

confidence: 88%

“…It is also well-recognized in some pediatric situations 27 . Pressure support ventilation (PSV) was chosen because literature has only one study investigating the attenuation of protein catabolic effects by using this ventilation mode 28 . This study analyzes diaphragmatic muscle atrophy and the PSV mode seems to preserve diaphragmatic muscle activity when compared with the CMV mode.…”

Section: Analysis Of Experimental Designmentioning

confidence: 99%

Effects of controlled and pressure support mechanical ventilation on rat diaphragm muscle

Oliveira

Costa²,

Assis

et al. 2012

Acta Cir. Bras.

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PURPOSE:The objective of this study was to analyze the effects of Pressure Controlled Ventilation mode (PCV-C) and PSV mode in diaphragm muscle of rats. METHODS: Wistar rats (n=18) were randomly assigned to the control group or to receive 6 hours of PCV and PSV. After this period, animals were euthanized and their diaphragms were excised, frozen in liquid nitrogen and stored in at -80º C for further histomorphometric analysis. RESULTS: Results showed a 15% decrease in cross-sectional area of muscle fibers on the PCV-C group when compared to the control group (p<0.001) and by 10% when compared to the PSV group (p<0.05). Minor diameter was decreased in PCV-C group by 9% when compared with the control group (p<0.001) and by 6% when compared to the PSV group (p<0.05). When myonuclear area was analyzed, a 16% decrease was observed in the PCV-C group when compared to the PSV group (p<0.05). No significant difference between the groups was observed in myonuclear perimeter (p>0.05). CONCLUSION: Short-term controlled mechanical ventilation seems to lead to muscular atrophy in diaphragm fibers. The PSV mode may attenuate the effects of VIDD. Key words: Anatomy & Histology. Diaphragm. Tracheostomy. Rats, Wistar. RESUMO OBJETIVO:Avaliar os efeitos do modo ventilatório controlado por pressão controlada (PCV-C) e do modo PSV sobre o músculo diafragma de ratos. MÉTODOS: Ratos (n = 18) da linhagem Wistar foram distribuídos no grupo controle (RE) ou para receber AVM por 6 horas no modo PCV-C e no modo PSV. Após esse período, os animais foram eutanasiados, o diafragma retirado e encaminhado para a análise histológica e morfométrica. RESULTADOS: Os resultados revelaram uma redução da área das fibras musculares de 15% no grupo PCV-C em comparação ao controle (p<0,001) e de 10% quando comparado ao grupo PSV (p<0,05). Já com relação ao diâmetro menor observou-se uma redução de 9% do grupo PCV-C em comparação ao controle (p<0,001) e de 6% em relação ao grupo PSV (p<0,05). Quando avaliada a área dos mionúcleos, notou-se uma redução de 16% desse parâmetro no grupo PCV-C, comparado ao PSV (p<0,05). Não houve diferença significativa no perímetro dos mionúcleos entre os grupos estudados (p>0,05). CONCLUSÃO: O grupo PCV-C apresentou atrofia muscular em um período curto de ventilação mecânica. O modo PSV parece atenuar os efeitos da DDIV.

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Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

Berger

Bloechlinger

Haehling

et al. 2016

J cachexia sarcopenia muscle

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Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed ‘ventilator‐induced diaphragmatic dysfunction’ (VIDD) and should be distinguished from peripheral muscular weakness as observed in ‘ICU‐acquired weakness (ICU‐AW)’.Interestingly, VIDD and ICU‐AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross‐sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.

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Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm

Cited by 125 publications

References 60 publications

Ventilator-induced diaphragm dysfunction: cause and effect

Ventilator-induced diaphragm dysfunction: cause and effect

Effects of controlled and pressure support mechanical ventilation on rat diaphragm muscle

Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

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