Sarcolemmal KATP Channel Triggers Opioid-Induced Delayed Cardioprotection in the Rat

H. Patel, A. Hsu, J. Peart, G. Gross
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引用次数: 55

Abstract

Recently, the involvement of sarcolemmal KATP (sarcKATP) channels in ischemic and pharmacological preconditioning (IPC and PPC) has been minimized by numerous studies suggesting a primary role for mitochondrial KATP (mitoKATP) channels in early and delayed cardioprotection. Although the mitoKATP channel has clearly been shown to be a distal effector of delayed IPC and PPC, studies implicating it as a trigger of protection in delayed IPC are lacking. Accordingly, we characterized the role of cardiac KATP channels as triggers or distal effectors of delayed cardioprotection induced by opioids in rats, and the data suggest that the sarcKATP channel triggers and that the mitoKATP channel is a distal effector of opioid-induced delayed cardioprotection.
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大鼠肌上皮KATP通道触发阿片类药物诱导的延迟心脏保护
最近,许多研究表明线粒体KATP (mitoKATP)通道在早期和延迟的心脏保护中起主要作用,从而最小化了肌层KATP (sarcKATP)通道在缺血和药物预处理(IPC和PPC)中的参与。虽然mitoKATP通道已被清楚地证明是延迟IPC和PPC的远端效应,但研究表明它在延迟IPC中作为保护的触发因素缺乏。因此,我们描述了大鼠心脏KATP通道作为阿片类药物诱导的延迟心脏保护的触发器或远端效应器的作用,数据表明sarcKATP通道触发和mitoKATP通道是阿片类药物诱导的延迟心脏保护的远端效应器。
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