Abstract
BackgroundMechanical ventilation (MV) induces diaphragmatic muscle fiber atrophy and contractile dysfunction (ventilator induced diaphragmatic dysfunction, VIDD). It is unknown how rapidly diaphragm muscle recovers from VIDD once spontaneous breathing is restored. We hypothesized that following extubation, the return to voluntary breathing would restore diaphragm muscle fiber size and contractile function using an established rodent model.MethodsFollowing 12 hours of MV, animals were either euthanized or, after full wake up, extubated and returned to voluntary breathing for 12 hours or 24 hours. Acutely euthanized animals served as controls (each n = 8/group). Diaphragmatic contractility, fiber size, protease activation, and biomarkers of oxidative damage in the diaphragm were assessed.Results12 hours of MV induced VIDD. Compared to controls diaphragm contractility remained significantly depressed at 12 h after extubation but rebounded at 24 h to near control levels. Diaphragmatic levels of oxidized proteins were significantly elevated after MV (p = 0.002) and normalized at 24 hours after extubation.ConclusionsThese findings indicate that diaphragm recovery from VIDD, as indexed by fiber size and contractile properties, returns to near control levels within 24 hours after returning to spontaneous breathing. Besides the down-regulation of proteolytic pathways and oxidative stress at 24 hours after extubation further repairing mechanisms have to be determined.
Highlights
Mechanical ventilation (MV) is a common intervention in intensive care units to provide adequate oxygenation of highly sedated patients or with respiratory failure
Four animals did not survive the full duration of MV due to tube blockade and hypoxemia, one animal (EXT24) was excluded for unnatural behavior and increased body temperature and was replaced
One animal in the CMV group died at the end of the experiment and was not replaced: data of CMV group pertains to 7 animals
Summary
Mechanical ventilation (MV) is a common intervention in intensive care units to provide adequate oxygenation of highly sedated patients or with respiratory failure. MV is a lifesaving intervention, prolonged MV results in diaphragmatic atrophy and contractile dysfunction, which is termed ventilatorinduced diaphragmatic dysfunction (VIDD). The failure to wean patients from MV is a significant clinical problem that prolongs time on the ventilator and increases morbidity and mortality [5]. It is important to understand how rapidly the diaphragm recovers from VIDD after the return to spontaneous breathing and extubation. Mechanical ventilation (MV) induces diaphragmatic muscle fiber atrophy and contractile dysfunction (ventilator induced diaphragmatic dysfunction, VIDD). It is unknown how rapidly diaphragm muscle recovers from VIDD once spontaneous breathing is restored. We hypothesized that following extubation, the return to voluntary breathing would restore diaphragm muscle fiber size and contractile function using an established rodent model
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