Mechanical ventilation promotes redox status alterations in the diaphragm.

@article{Falk2006MechanicalVP,
  title={Mechanical ventilation promotes redox status alterations in the diaphragm.},
  author={Darin J. Falk and Keith C. Deruisseau and Darin van Gammeren and Melissa A. Deering and Andreas N. Kavazis and Scott K Powers},
  journal={Journal of applied physiology},
  year={2006},
  volume={101 4},
  pages={
          1017-24
        }
}
Oxidative stress is an important mediator of diaphragm muscle atrophy and contractile dysfunction during prolonged periods of controlled mechanical ventilation (MV). To date, specific details related to the impact of MV on diaphragmatic redox status remain unknown. To fill this void, we tested the hypothesis that MV-induced diaphragmatic oxidative stress is the consequence of both an elevation in intracellular oxidant production in conjunction with a decrease in the antioxidant buffering… 
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It is demonstrated that prolonged MV results in increased diaphragmatic expression of a key stress-sensitive enzyme, heme oxygenase (HO)-1, and tested the hypothesis that HO-1 acts as a pro-oxidant in thediaphragm during prolonged MV, finding that it is neither a pro -oxidants nor an antioxidant in the diaphagm during MV.
Xanthine oxidase contributes to mechanical ventilation-induced diaphragmatic oxidative stress and contractile dysfunction.
TLDR
The failure of XO inhibition to completely prevent MV-induced diaphragmatic oxidative damage suggests that other sources of oxidant production are active in the diaphragem during prolonged MV.
Mechanical ventilation induces diaphragmatic mitochondrial dysfunction and increased oxidant production.
Increased SOD2 in the diaphragm contributes to exercise-induced protection against ventilator-induced diaphragm dysfunction
Mitochondria-targeted antioxidants protect against mechanical ventilation-induced diaphragm weakness*
TLDR
Results reveal that prevention of mechanical ventilation-induced increases in diaphragmatic mitochondrial reactive oxygen species emission protects the diphragm from mechanical ventilation -induced diaphagmatic weakness, and indicates that mitochondria are a primary source of reactive oxygen Species production in the diaphragem during prolonged mechanical ventilation.
N-Acetylcysteine protects the rat diaphragm from the decreased contractility associated with controlled mechanical ventilation*
TLDR
The administration of N-acetylcysteine prevents against controlled mechanical ventilation-induced diaphragmatic oxidative stress and proteolysis and abolishes controlled mechanical ventilator-induceddiaphragm contractile dysfunction.
The chaperone co-inducer BGP-15 alleviates ventilation-induced diaphragm dysfunction
TLDR
An experimental intensive care unit (ICU) model was used, allowing time-resolved studies of diaphragm structure and function in response to long-term mechanical ventilation and the effects of a pharmacological intervention (the chaperone co-inducer BGP-15).
Ventilator-induced diaphragm dysfunction: the clinical relevance of animal models
TLDR
The major clinical implication of the VIDD is to limit the use of CMV to the extent possible, since partial (assisted) modes of ventilatory support should be used whenever feasible, since these modes attenuate the deleterious effects of mechanical ventilation on respiratory muscles.
Redox homeostasis, oxidative stress and disuse muscle atrophy
TLDR
It is hypothesised that in some muscles, models and species only, due to a large redox imbalance, the leading phenomena are activation of proteolysis and massive oxidation of proteins, which would become more susceptible to degradation.
Relevance of Ventilator-induced Diaphragm Dysfunction in ICU Patients
TLDR
Although VIDD is a well-demonstrated phenomenon in animal models for controlled MV, its relevance in MV patients in the ICU remains questionable and large-scale studies in humans are needed to establish the actual role of MV in the pathogenesis of an ICU-acquired diaphragm dysfunction.
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