Anesthesiology
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Ischemia-reperfusion injury causes chronic postischemia pain (CPIP), and rats with higher glycemia during ischemia-reperfusion injury exhibit increased allodynia. Glycemia-induced elevation of nuclear factor κB (NFκB) may contribute to increased allodynia. ⋯ NFκB was activated in a glycemia-dependent manner in CPIP rats. Hypoglycemic rats were more sensitive to SN50 than rats with higher glycemia. The finding that SN50 reduces mechanical allodynia suggests that NFκB inhibitors might be useful for treating postischemia pain.
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Oxidative stress is implicated in pathogenesis of cardiac reperfusion injury, characterized by cellular Ca2+ overload and hypercontracture. Volatile anesthetics protect the heart against reperfusion injury primarily by attenuating Ca2+ overload. This study investigated electrophysiological mechanisms underlying cardioprotective effects of sevoflurane against oxidative stress-induced cellular injury. ⋯ Sevoflurane protected ventricular myocytes against H2O2-induced Ca2+ overload and hypercontracture, presumably by affecting multiple Ca2+ transport pathways, including ICa,L, Na+/Ca2+ exchanger and ryanodine receptor. These actions appear to mediate cardioprotection against reperfusion injury associated with oxidative stress.
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Unilateral acid aspiration augments the effects of ventilator lung injury in the contralateral lung.
Mechanical ventilation is necessary during acute respiratory distress syndrome, but it promotes lung injury because of the excessive stretch applied to the aerated parenchyma. The authors' hypothesis was that after a regional lung injury, the noxious effect of mechanical ventilation on the remaining aerated parenchyma would be more pronounced. ⋯ Aggressive mechanical ventilation aggravates the preexisting lung injury, which is noxious for the contralateral, not previously injured lung, possibly because of a regional redistribution of VT.