Key result
Isoflurane pretreatment cuts oxidative cardiomyocyte death ~45% via sarcolemmal and mitochondrial K(ATP) channels.
Why the study?
It is unclear whether sarcolemmal and mitochondrial K(ATP) channels act as triggers or effectors in isoflurane-induced cardiac preconditioning against oxidative stress.
Population
Adult rat cardiomyocytes exposed to oxidative stress with 200 microM H2O2 and 100 microM FeSO4
Comparison
Isoflurane pretreatment with or without sarcolemmal and mitochondrial K(ATP) channel inhibitors
Design
Preclinical experimental study
Authors
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Role of K(ATP) channels in anesthetic preconditioning remains unclear; leaves open their precise role as triggers or effectors.
Absolute Event Rate: 26% vs 47%
Isoflurane-induced cardioprotection against oxidative stress involves sarcolemmal K(ATP) channels acting as effectors and mitochondrial K(ATP) channels acting as both triggers and effectors.
Marinović et al. (2006) studied Oxidative stress / Ischemia-reperfusion injury. Isoflurane pretreatment vs. Oxidative stress without pretreatment was evaluated on Cell death. Isoflurane pretreatment attenuated oxidative stress-induced cell death in adult rat cardiomyocytes from 47% to 26%, a protective effect dependent on sarcolemmal and mitochondrial K(ATP) channels.
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