British journal of anaesthesia
Sevoflurane protects the myocardium against ischaemic injury through protein kinase C (PKC) activation, mitochondrial K+ATP-channel (mitoK+ATP) opening and production of reactive oxygen species (ROS). However, it is unclear whether the type of ischaemia determines the involvement of these signalling molecules. We therefore investigated whether hypoxia (HYP) or metabolic inhibition (MI), which differentially inhibit the mitochondrial electron transport chain (ETC), are comparable concerning the relative contribution of PKC, mitoK+ATP and ROS in sevoflurane-induced cardioprotection. ⋯ PKC, mitoK+ATP and ROS are involved in sevoflurane-induced cardioprotection after HYP or MI, suggesting that the means of mitochondrial ETC inhibition does not determine the signal transduction pathway for cardioprotection by anaesthetics.