Effects of mechanical ventilation on diaphragm function and biology

Gayan‐Ramirez, Ghislaine; Decramer, Marc

doi:10.1183/09031936.02.00063102

Cited by 86 publications

(62 citation statements)

References 45 publications

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“…Although controversy exists, it has been predicted that depressed strength and endurance of respiratory muscles can play a key role in weaning difficulties (26,34,115). However, direct evidence demonstrating cause and effect that VIDD is primarily responsible for weaning problems is lacking due to the difficulty of performing these experiments in humans.…”

Section: Contribution Of Vidd To Weaning Failurementioning

confidence: 99%

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: Contribution Of Vidd To Weaning Failurementioning

confidence: 99%

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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“…The techniques used to alter tissue load are extremely diverse but can be separated into two categories based on their effect: decreased muscle activity (DMA) and increased muscle activity (IMA). Examples of DMA are reduced electrical activity through spinal cord isolation and the use of neurotoxins, spinal cord injury or transection, unloading (mainly of the hindlimb), immobilisation of muscle in a shortened position, space flight, mechanical ventilation and bed rest (Carlson et al, 1999;Gayan-Ramirez and Decramer, 2002;Lalani et al, 2000;Talmadge, 2000;Wehling et al, 2000). Examples of IMA are endurance (swim) training and chronic low-frequency stimulation of muscles (CLFS) (De Graaf et al, 1990;Kraus and Pette, 1997;Pette, 1998;Siu et al, 2004;Walker et al, 2004).…”

Section: Gene Expression Levelsmentioning

confidence: 99%

Effects of decreased muscle activity on developing axial musculature innicb107mutant zebrafish (Danio rerio)

Meulen

Schipper

Leeuwen

et al. 2005

Journal of Experimental Biology

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SUMMARY The present paper discusses the effects of decreased muscle activity (DMA)on embryonic development in the zebrafish. Wild-type zebrafish embryos become mobile around 18 h post-fertilisation, long before the axial musculature is fully differentiated. As a model for DMA, the nicb107mutant was used. In nicb107 mutant embryos, muscle fibres are mechanically intact and able to contract, but neuronal signalling is defective and the fibres are not activated, rendering the embryos immobile. Despite the immobility, distinguished slow and fast muscle fibres developed at the correct location in the axial muscles, helical muscle fibre arrangements were detected and sarcomere architecture was generated. However, in nicb107 mutant embryos the notochord is flatter and the cross-sectional body shape more rounded, also affecting muscle fibre orientation. The stacking of sarcomeres and myofibril arrangement show a less regular pattern. Finally, expression levels of several genes were changed. Together, these changes in expression indicate that muscle growth is not impeded and energy metabolism is not changed by the decrease in muscle activity but that the composition of muscle is altered. In addition, skin stiffness is affected. In conclusion, the lack of muscle fibre activity did not prevent the basal muscle components developing but influenced further organisation and differentiation of these components.

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“…The level of this strength reduction is related to duration of MV (Chang, Boots, Brown, et al, 2005;Powers et al, 2002;Sassoon, Caiozzo et al, 2002;Sprague & Hopkins, 2003) and has been reported as one of the major determinants of weaning failure in patients receiving MV (N Ambrosino, 2005;Gayan-Ramirez & Decramer, 2002). Anzueto et al (Anzueto, et al, 1997) observed a transdiaphragmatic pressure reduction of 45% in rats after 11 days of controlled MV.…”

Section: Respiratory Muscle Trainingmentioning

confidence: 99%