Abstract
Summary With controlled mechanical ventilation (CMV) the diaphragm is inactive. The application of short-term CMV at the onset of cardiogenic shock or sepsis exerts protective effects on the diaphragm muscle. On the other hand, CMV can produce detrimental effects on healthy diaphragm muscle. The effects are rapid and progressive, and are associated with either muscle atrophy or myofibril damage; the mechanisms of both involve decreased protein synthesis and increased contractile protein degradation. Protein degradation is mediated via interactive molecular signaling, including oxidative stress, apoptosis, and proteasome-proteolysis. Auspiciously, strategies to maintain partial diaphragmatic contractions can mitigate ventilator-induced diaphragmatic dysfunction.
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