Sevoflurane-induced cardioprotection depends on PKC-α activation via production of reactive oxygen species

Sevoflurane improves post-ischaemic contractile recovery via activation of PKC-α. ROS production, but not opening of mitoK+ATP channels, precedes PKC-α translocation towards mitochondria. This study shows the involvement of Ca2+-dependent PKC-α in addition to the well-established role of Ca2+-independent PKC isoforms in sevoflurane-induced cardioprotection.