Effects of controlled mechanical ventilation on respiratory muscle contractile properties in rabbits

Capdevila, Xavier; Lopez, Sandrine; Bernard, Nathalie; Rabischong, E.; Ramonatxo, M; Martinazzo, Guilhem; Préfaut, Christian

doi:10.1007/s00134-002-1548-3

Cited by 94 publications

(74 citation statements)

References 34 publications

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“…Importantly, these results suggest that the MV-induced diaphragm contractile dysfunction occurs at the level of the peripheral muscle (91). Indeed, numerous animal studies consistently report that prolonged MV results in a rapid and time-dependent decrease in diaphragmatic specific force production measured in vitro using electrical stimulation of diaphragmatic muscle strips (9,16,19,33,35,56,87,93,98). A recent report suggests that as few as 6 h of MV results in diaphragmatic contractile dysfunction in mice (73).…”

Section: Mv-induced Diaphragmatic Contractile Dysfunctionmentioning

confidence: 87%

“…This primate study concluded that prolonged MV results in significant impairment of diaphragmatic contractile performance as indicated by a decrease in both maximal transdiaphragmatic pressure and diaphragmatic endurance (6). Following these early investigations, scientific interest in the effects of MV on diaphragm structure and function grew rapidly, and numerous animal studies published in 2002-2003 consistently concluded that prolonged MV results in the rapid development of both diaphragmatic atrophy and contractile dysfunction (16,19,33,91,93,98,100). Mechanistic studies into the cell signaling events responsible for VIDD began in 2003 when investigations revealed that prolonged MV results in diaphragmatic oxidative stress and that oxidant damage in the diaphragm is a requirement for VIDD (9,119).…”

Section: Ventilator-induced Diaphragm Dysfunction: Historical Overviewmentioning

confidence: 97%

“…Numerous animal studies using a variety of species (mice, rats, rabbits, and pigs) have reported that prolonged MV results in significant atrophy of diaphragm muscle fibers (16,49,73,78,100,107). However, because the rat and human diaphragm are anatomically alike and contain a similar fiber type composition (76,81), the rat has become the most commonly used animal model to study MV-induced changes in diaphragm fiber size and function.…”

Section: Mv-induced Diaphragm Atrophymentioning

confidence: 99%

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Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

139

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 Diaphragmatic Contractile Dysfunctionmentioning

confidence: 87%

Section: Ventilator-induced Diaphragm Dysfunction: Historical Overviewmentioning

confidence: 97%

Section: Mv-induced Diaphragm Atrophymentioning

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

139

156

View full text Add to dashboard Cite

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“…Studies demonstrated the following alterations in the diaphragm after controlled mechanical ventilation: reduced muscle mass 2,10,11 ; diminished type I, IIa, and IIx/b fiber dimensions 3,12,13 ; myofibrillar damage 4 ; enhanced proteolysis 12 ; increased protein oxidation and lipid peroxidation 14 ; reduced expression of the insulin-like growth factor (IGF-I) 3 ; decreased sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase (SERCA-1a) expression 15 ; increased expression of muscle atrophy factor (MAF-box) 16 ; and a decrease in myonuclear content 17 . All of these factors seem to contribute to the development of VIDD, but the precise contribution of each factor and their apparition kinetics has yet to be defined.…”

Section: Ventilator-induced Diaphragmatic Dysfunction (Vidd)mentioning

confidence: 99%

“…Controlled mechanical ventilation induces diaphragm muscle atrophy [10][11][12][13] . VIDD develops rapidly, as early as 12 h after the institution of CMV 17 , and is more pronounced in the diaphragm, which atrophies earlier than the peripheral skeletal muscles that are also inactive during CMV [10][11][12] .…”

Section: Muscle Atrophymentioning

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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Effects of controlled mechanical ventilation on respiratory muscle contractile properties in rabbits

Abstract: Mechanical ventilation in rabbits produces alterations in contractile properties of the diaphragm and 5th external intercostal muscle, increases both muscles fatigue, and promotes atrophy of type II fibers.

Cited by 94 publications

References 34 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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