Presence of store-operated Ca2+ entry in C57BL/6J mouse ventricular myocytes and its suppression by sevoflurane

Sevoflurane at concentrations of ≥2% significantly inhibits the SOCE activity and prevents the resultant cellular Ca2+ overload that leads to hypercontracture in ventricular myocytes. This inhibitory action may be involved in the cardioprotective effect of sevoflurane against Ca2+ overload-mediated injury.