Anesthesiology
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Comparative Study
Negative Pressure Ventilation and Positive Pressure Ventilation Promote Comparable Levels of Ventilator-induced Diaphragmatic Dysfunction in Rats.
Mechanical ventilation is a life-saving intervention for patients with respiratory failure. Unfortunately, a major complication associated with prolonged mechanical ventilation is ventilator-induced diaphragmatic atrophy and contractile dysfunction, termed ventilator-induced diaphragmatic dysfunction (VIDD). Emerging evidence suggests that positive pressure ventilation (PPV) promotes lung damage (ventilator-induced lung injury [VILI]), resulting in the release of signaling molecules that foster atrophic signaling in the diaphragm and the resultant VIDD. Although a recent report suggests that negative pressure ventilation (NPV) results in less VILI than PPV, it is unknown whether NPV can protect against VIDD. Therefore, the authors tested the hypothesis that compared with PPV, NPV will result in a lower level of VIDD. ⋯ These results demonstrate that NPV and PPV result in similar levels of VILI and that NPV and PPV promote comparable levels of VIDD in rats.
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Oxidative stress is implicated in pathogenesis of cardiac reperfusion injury, characterized by cellular Ca overload and hypercontracture. Volatile anesthetics protect the heart against reperfusion injury primarily by attenuating Ca overload. This study investigated electrophysiological mechanisms underlying cardioprotective effects of sevoflurane against oxidative stress-induced cellular injury. ⋯ Sevoflurane protected ventricular myocytes against H2O2-induced Ca overload and hypercontracture, presumably by affecting multiple Ca transport pathways, including ICa,L, Na/Ca exchanger and ryanodine receptor. These actions appear to mediate cardioprotection against reperfusion injury associated with oxidative stress.