Developmental myosin heavy chains in the adult human diaphragm: coexpression patterns and effect of COPD

Nguyen, Taitan; Shrager, Joseph B.; Kaiser, Larry R.; Mei, Lijuan; Daood, Monica J.; Watchko, Jon F.; Rubinstein, Neal A.; Levine, Stephen B.

doi:10.1152/jappl.2000.88.4.1446

Cited by 36 publications

(37 citation statements)

References 46 publications

(48 reference statements)

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“…The proportion of MyHC-I fibres in the non-COPD group Glu mmol·kg WW -1 lis somewhat higher than those previously reported by NGUYEN et al [34] and LEVINE and coworkers [6,35] (45 and 41%). This may be related to differences in the criteria used for selection of a control group.…”

Section: Glutathione Concentration In Relation To Fibre Typecontrasting

confidence: 56%

“…The possibility that the presence of lung cancer contributes to the slightly higher level of MyHC-I fibres in the diaphragm cannot be totally excluded, although the exact underlying mechanism is difficult to elucidate. NGUYEN et al [34] and LEVINE and coworkers [6,35] included subjects with mild pulmonary impairment undergoing resection of solitary pulmonary nodules and brain-dead organ donors. It is possible that both the underlying lung diseases in the first group and the amount of time in receipt of ventilatory support and the decreased central ventilatory drive due to brain death in the second group may be an important bias.…”

Section: Glutathione Concentration In Relation To Fibre Typementioning

confidence: 99%

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Glutathione and glutamate levels in the diaphragm of patients with chronic obstructive pulmonary disease

Engelen¹,

Orozco-Levi²,

Deutz³

et al. 2004

European Respiratory Journal

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Recently, decreased glutamate (Glu) and reduced glutathione (GSH) levels were reported in the quadriceps femoris of patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate whether Glu and GSH levels are also modified in the diaphragm of these patients.Nine male COPD patients (forced expiratory volume in one second (FEV1) range 28-68% of the predicted value) and seven male patients with normal pulmonary function (mean¡SD FEV1 86¡3% pred) submitted to thoracotomy were included. Biopsy specimens were taken from the diaphragm (both groups) and the quadriceps femoris (COPD group alone) in order to assess fibre size, myosin heavy chain expression, GSH levels and amino acid profile.The COPD group was characterised by preserved fibre size, a higher proportion of type I fibres (mean¡SEM 70¡3 versus 26¡4%), and higher Glu and GSH content in the diaphragm compared to the quadriceps muscle. However, Glu and GSH levels were similar in diaphragm from the COPD and control groups. Glu level correlated with GSH level in both muscles. No significant correlation was found between Glu or GSH level and fibre size or proportions.This study shows that glutamate and reduced glutathione levels are preserved in the diaphragm of chronic obstructive pulmonary disease patients. Alterations in glutamate and reduced glutathione metabolism are muscle-specific in chronic obstructive pulmonary disease, affecting the quadriceps femoris but not the diaphragm. Glutamate and reduced glutathione levels are strongly interrelated in both muscles, independent of fibre type distribution and fibre size.

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Section: Glutathione Concentration In Relation To Fibre Typecontrasting

confidence: 56%

Section: Glutathione Concentration In Relation To Fibre Typementioning

confidence: 99%

Glutathione and glutamate levels in the diaphragm of patients with chronic obstructive pulmonary disease

Engelen¹,

Orozco-Levi²,

Deutz³

et al. 2004

European Respiratory Journal

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“…No fall in Pdi,tw was observed in either study, suggesting that the diaphragm is relatively fatigue resistant in COPD. This is supported by the observation that COPD patients appear to be better at sustaining maximum voluntary ventilation than normal subjects [111] and, indeed, histologically, the cellular adaptations of the diaphragm in COPD show an increased proportion of type I slow muscle fibres or slow myosin heavy-chain isoforms [112]. With this in mind, it is unsurprising that the effects of inspiratory muscle training in COPD remain controversial.…”

Section: Chronic Obstructive Pulmonary Diseasementioning

confidence: 91%

Magnetic stimulation for the measurement of respiratory and skeletal muscle function

Man¹

2004

European Respiratory Journal

117

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Respiratory and skeletal muscle function is of interest in many areas of pulmonary and critical care medicine. The capacity of the respiratory muscle pump to respond to the load imposed by disease is the basis of an understanding of ventilatory failure. Over the last four decades, considerable progress has been made in quantifying the capacity of the respiratory muscles, in terms of strength, endurance and fatigue. With the development of magnetic stimulation, it has recently become possible to nonvolitionally assess the respiratory muscles in a clinically acceptable way. This is of particular interest in the investigation of patients receiving critical care, those with neuromuscular disease, and in children where volitional efforts are either not possible or likely to be sub-maximal. Furthermore, the adaptation of these techniques to quantify the strength of peripheral muscles, such as the quadriceps, has allowed the effects of muscle training or rehabilitation, uninfluenced by learning effect, to be assessed. This article focuses on the physiological basis of magnetic nerve stimulation, and reviews how the technique has been applied to measure muscle strength and fatigue, with particular emphasis upon the diaphragm. The translation of magnetic stimulation into a clinical tool is described, and how it may be of diagnostic, prognostic and therapeutic value in several areas of pulmonary medicine. In particular, the use of magnetic stimulation in neuromuscular disease, the intensive care setting, chronic obstructive pulmonary disease and paediatrics will be discussed. The nonvolitional assessment of skeletal musclesFor routine muscle strength measurements, the force generated from a maximum voluntary contraction (MVC) is often used. However volitional, effort-dependent manoeuvres for measuring strength are not always suitable for patients as the ability to perform a true MVC relies upon subject motivation and cooperation. This is particularly so in patients on intensive care units (ICU), children, patients with cognitive difficulties, and those patients prevented from performing a true MVC by pain (for example, following surgery). However, even in well-motivated subjects, sub-maximal muscle activation is common in routine clinical practice [1]. As volitional manoeuvres are influenced by a learning effect, the value of MVC is also limited in studies of training or rehabilitation. Consequently, there has been a need for nonvolitional methods to assess muscle strength. Skeletal muscle physiologySkeletal muscle is controlled by electrical impulses conducted by motor neurones that lead to the release of acetylcholine from the motor end plate, thus depolarising the muscle cell membrane. The force generated by muscle contraction is dependent upon a number of factors, including the number of muscle fibres stimulated, muscle length at the time of stimulation and the frequency of stimulation. The force-frequency curve of a muscle is of particular relevance in the understanding of nonvolitional techniques to asse...

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“…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. Several studies reveal that as few as 12 h of controlled MV results in a 10 -15% reduction in the cross-sectional area of all rat diaphragm fiber types (i.e., type I, type IIa, and type IIx/b) (67,69,82,103).…”

Section: Mv-induced Diaphragm Atrophymentioning

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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Developmental myosin heavy chains in the adult human diaphragm: coexpression patterns and effect of COPD

Cited by 36 publications

References 46 publications

Glutathione and glutamate levels in the diaphragm of patients with chronic obstructive pulmonary disease

Glutathione and glutamate levels in the diaphragm of patients with chronic obstructive pulmonary disease

Magnetic stimulation for the measurement of respiratory and skeletal muscle function

Ventilator-induced diaphragm dysfunction: cause and effect

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