Ca~(2+)、PROTEIN KINASE C IN RAT HEARTS AND ISCHEMIC PRECONDITIONING

Objective:To investigated the role of [Ca~2+] 1 and protein kinase C (PKC) by using the isolated rat heart in the cardioprotection mechanism of ischemic preconditioning(IPC).Methods:Sixty four Sprague-Dawley male rats were divided into eight groups randomly. Langendorff-perfused rat hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion (I/R). We observe the change of cardioprotection effects with different pretreatment.Results:A significant functional recovery and lactate dehydrogenase release were observed in IPC rat hearts compared with ischemic control hearts. ATP contents of IPC hearts was significantly higher than those of ischemic control hearts. Pretreatment with Bay K 8644, a L-type Ca~2+-channel opener, could mimic IPC-induced protection. Verapamil administrated during IPC and Bay K 8644 groups attenuated the IPC-induced protection effects. Administrated of Chelerythrine, a specific PKC inhibitor, completely abolished IPC-induced protection both in IPC and Bay K 8644 groups.Conclusion:A transient increase in [Ca~2+] 1 during IPC and Bay K 8644 groups is an important trigger for the activation of PKC, which is responsible for cardioprotection.