Oxidative Stress and Respiratory Muscle Dysfunction in Severe Chronic Obstructive Pulmonary Disease

Barreiro, Esther; Puente, Beatriz de la; Minguella, Joan; Corominas, Josep M.; Serrano, Sergi; Hussain, Sabah N. A.; Gea, Joaquim

doi:10.1164/rccm.200407-887oc

Cited by 215 publications

(205 citation statements)

References 39 publications

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“…There is a large body of evidence, much of which is beyond the scope of this review, which supports the view that skeletal muscle dysfunction is a major contributor to exercise limitation in COPD [50][51][52][53][54]. It could therefore be hypothesised that the effects observed on muscle performance in nonanaemic athletes with EPO may also be seen in COPD patients.…”

Section: Skeletal Muscle Functionsupporting

confidence: 55%

The potential impact of anaemia of chronic disease in COPD

Similowski

Agustí²,

MacNee³

et al. 2006

Eur Respir J

153

107

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Anaemia of chronic disease (ACD), with chronically low levels of circulating haemoglobin, is an immune driven abnormality that occurs in many inflammatory diseases, and also in chronic heart failure. Although chronic obstructive pulmonary disease (COPD) is ''traditionally'' associated with polycythaemia, the systemic inflammation that is now recognised as a feature of COPD makes it a possible cause of ACD. If present in COPD, anaemia could worsen dyspnoea and limit exercise tolerance.Preliminary evidence suggests that anaemia in COPD patients may be more prevalent than expected, concerning 10-15% of patients suffering from severe forms of the disease. A database study conducted in 2,524 COPD patients being prescribed long-term oxygen therapy has shown that a low haematocrit is a strong predictor of survival in this population, before body mass index, and is associated with more hospitalisations and a longer cumulative duration of hospitalisation. COPD patients with low haemoglobin levels have a poorer prognosis than COPD patients with normal haemoglobin levels in the event of acute gastrointestinal bleeding or after elective aneurysm repair. Raising haemoglobinaemia through transfusion decreases minute ventilation and work of breathing in COPD patients.These preliminary evidences point to the need to study the prevalence of anaemia, and its physiological and clinical impact in chronic obstructive pulmonary disease. When this body of knowledge is available, the question of the putative benefits of raising haemoglobinaemia in chronic obstructive pulmonary disease will have to be addressed.

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Section: Skeletal Muscle Functionsupporting

confidence: 55%

The potential impact of anaemia of chronic disease in COPD

Similowski

Agustí²,

MacNee³

et al. 2006

Eur Respir J

153

107

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“…Oxidative stress may be enhanced in skeletal muscle of COPD patients as peroxidation products are elevated in the plasma of COPD patients at rest, after submaximal exercise and during exacerbations of the disease [86]. ROS can increase muscle proteolysis, inhibit muscle-specific protein expression and increase muscle cell apoptosis [87]. Skeletal muscle biopsies from COPD patients show increased protein carbonylation as evidence of increased oxidative stress [88].…”

Section: Mechanismsmentioning

confidence: 99%

Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

Eur Respir J

1,476

1,113

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Increasing evidence indicates that chronic obstructive pulmonary disease (COPD) is a complex disease involving more than airflow obstruction. Airflow obstruction has profound effects on cardiac function and gas exchange with systemic consequences. In addition, as COPD results from inflammation and/or alterations in repair mechanisms, the ''spill-over'' of inflammatory mediators into the circulation may result in important systemic manifestations of the disease, such as skeletal muscle wasting and cachexia. Systemic inflammation may also initiate or worsen comorbid diseases, such as ischaemic heart disease, heart failure, osteoporosis, normocytic anaemia, lung cancer, depression and diabetes. Comorbid diseases potentiate the morbidity of COPD, leading to increased hospitalisations, mortality and healthcare costs. Comorbidities complicate the management of COPD and need to be evaluated carefully. Current therapies for comorbid diseases, such as statins and peroxisome proliferator-activated receptor-agonists, may provide unexpected benefits for COPD patients. Treatment of COPD inflammation may concomitantly treat systemic inflammation and associated comorbidities. However, new broad-spectrum anti-inflammatory treatments, such as phosphodiesterase 4 inhibitors, have significant side-effects so it may be necessary to develop inhaled drugs in the future. Another approach is the reversal of corticosteroid resistance, for example with effective antioxidants. More research is needed on COPD comorbidities and their treatment.

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“…In the hamster model of emphysema, Heunks et al (32) demonstrated an elevation in glutathione oxidation state in the diaphragms of emphysematous hamsters compared with controls that was significantly correlated to the loss of maximum specific force. Barreiro et al (2) have reported elevations in markers of oxidative stress in diaphragms of patients with severe COPD, including increased protein carbonyl formation and hydroxynonenal-protein adducts, which are related to severity of disease and/or loss of respiratory muscle strength. These findings were recently corroborated in the diaphragms of patients with severe emphysema, which identified oxidation of specific proteins, including creatine kinase and contractile and cytoskeletal proteins within the sarcomere (51).…”

Section: Evidence For Respiratory Muscle Injury Protein Degradationmentioning

confidence: 99%

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

Clanton¹,

Levine²

2009

Journal of Applied Physiology

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Clanton TL, Levine S. Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation? J Appl Physiol 107: 324 -335, 2009. First published April 9, 2009 doi:10.1152/japplphysiol.00173.2009.-The diaphragm and other respiratory muscles undergo extensive remodeling in both animal models of emphysema and in human chronic obstructive pulmonary disease, but the nature of the remodeling is different in many respects. One common feature is a shift toward improved endurance characteristics and increased oxidative capacity. Furthermore, both animals and humans respond to chronic hyperinflation by diaphragm shortening. Although in rodent models this clearly arises by deletion of sarcomeres in series, the mechanism has not been proven conclusively in human chronic obstructive pulmonary disease. Unique characteristics of the adaptation in human diaphragms include shifts to more predominant slow, type I fibers, expressing slower myosin heavy chain isoforms, and type I and type II fiber atrophy. Although some laboratories report reductions in specific force, this may be accounted for by decreases in myosin heavy chain content as the muscles become more oxidative and more efficient. More recent findings have reported reductions in Ca 2ϩ sensitivity and reduced myofibrillar elastic recoil. In contrast, in rodent models of disease, there is no consistent evidence for loss of specific force, no consistent shift in fiber populations, and atrophy is predominantly seen only in fast, type IIX fibers. This review challenges the hypothesis that the adaptations in human diaphragm represent a form of dysfunction, secondary to systemic disease, and suggest that most findings can as well be attributed to adaptive processes of a complex muscle responding to unique alterations in its working environment. diaphragm; fiber type; sarcomere; skeletal muscle; emphysema THIS REVIEW IS INTENDED TO bring readers up to date with accumulating evidence that the diaphragm undergoes remarkable adaptations to chronic hyperinflation and chronic lung obstruction. Some of these adaptations are expected, based on well known responses of limb muscle to chronic changes in length and mechanical load, but others appear to be surprisingly unique, revealing aspects of muscle plasticity and pathology that are not anticipated from known basic science concepts. We will concentrate this review on what has been observed, primarily at the muscle fiber level in both animals and humans, with primary emphasis on the diaphragm. There have been several excellent previous reviews of this area, and the reader is encouraged to refer to these (13,41,58,65,66). Where possible, we will attempt to complement, update, and at times challenge current concepts with the purpose of furthering dialogue and promoting further inquiry. LENGTH PLASTICITYThe diaphragm, like all other muscles, exhibits a characteristic length-tension relationship analogous to the Frank-Starling curve for the heart. As length is increased in the relaxed muscle, a passive length-tension cu...

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Oxidative Stress and Respiratory Muscle Dysfunction in Severe Chronic Obstructive Pulmonary Disease

Abstract: This study shows that oxidative stress rather than nitric oxide is likely to be involved in the respiratory muscle dysfunction in severe COPD.

Cited by 215 publications

References 39 publications

The potential impact of anaemia of chronic disease in COPD

The potential impact of anaemia of chronic disease in COPD

Systemic manifestations and comorbidities of COPD

Respiratory muscle fiber remodeling in chronic hyperinflation: dysfunction or adaptation?

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