Anesthesiology
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Randomized Controlled Trial Clinical Trial
Variable ventilation improves perioperative lung function in patients undergoing abdominal aortic aneurysmectomy.
Optimizing perioperative mechanical ventilation remains a significant clinical challenge. Experimental models indicate that "noisy" or variable ventilation (VV)--return of physiologic variability to respiratory rate and tidal volume--improves lung function compared with monotonous control mode ventilation (CV). VV was compared with CV in patients undergoing abdominal aortic aneurysmectomy, a patient group known to be at risk of deteriorating lung function perioperatively. ⋯ The VV mode of ventilation significantly improved lung function over CV in patients undergoing abdominal aortic aneurysmectomy.
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Anesthetic preconditioning protects against cardiac ischemia/reperfusion injury. Increases in reduced nicotinamide adenine dinucleotide and reactive oxygen species during sevoflurane exposure suggest attenuated mitochondrial electron transport as a trigger of anesthetic preconditioning. The authors investigated the effects of sevoflurane on respiration in isolated cardiac mitochondria. ⋯ The findings suggest that sevoflurane-induced attenuation of complex I is mediated by reactive oxygen species, whereas attenuation of other respiratory complexes is mediated by a different mechanism. The opening of mitochondrial K(ATP) channels by sevoflurane does not seem to be involved in this effect. Thus, reactive oxygen species formation may not only result from attenuated electron transport by sevoflurane, but it may also contribute to complex I attenuation, possibly leading to a positive feedback and amplification of sevoflurane-induced reactive oxygen species formation in triggering anesthetic preconditioning.
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The authors tested the hypothesis that pretreatment with isoflurane or sevoflurane can protect the heart against neutrophil-induced contractile dysfunction. ⋯ Isoflurane and sevoflurane preconditioned the heart against neutrophil-induced contractile dysfunction. This action was associated with an inhibition to neutrophil adherence and likely involved an increased resistance of the myocardium to oxidant-induced injury; the adenosine triphosphate-sensitive potassium channels played no apparent role.