Nakano A, Cohen M V, Downey J M
Department of Physiology, MSB 3024, College of Medicine, University of South Alabama, Mobile, AL 36688, USA.
Pharmacol Ther. 2000 Jun;86(3):263-75. doi: 10.1016/s0163-7258(00)00058-9.
When the heart is subjected to a transient nonlethal period of ischemia, it quickly adapts itself to become resistant to infarction from a subsequent ischemic insult. This adaptation is called preconditioning. This cardioprotection has been shown to be mediated by stimulation of receptors linked to protein kinase C (PKC) (adenosine, bradykinin, opioids, etc.), and these receptors protect by activating PKC. PKC appears to be the first element of a complex kinase cascade that is activated during the prolonged ischemia in the preconditioned heart. Recent studies imply that p38 mitogen-activated protein kinase carries the signal from PKC to the mitochondrial K(ATP) channels, causing them to open and thus protect the heart. The cardioprotection of preconditioning occurs in all species tested to date, and possibly also humans. It is expected that as the mechanism of preconditioning is more thoroughly understood, pharmacological preconditioning will become practical for clinical use.
当心脏经历短暂的非致死性缺血期时，它会迅速自我适应，从而对随后的缺血性损伤产生梗死抗性。这种适应被称为预处理。已证明这种心脏保护作用是由与蛋白激酶C（PKC）相关的受体（腺苷、缓激肽、阿片类物质等）的刺激介导的，并且这些受体通过激活PKC来发挥保护作用。PKC似乎是在预处理心脏的长时间缺血过程中被激活的复杂激酶级联反应的第一个元件。最近的研究表明，p38丝裂原活化蛋白激酶将信号从PKC传递至线粒体ATP敏感性钾通道，使其开放，从而保护心脏。预处理的心脏保护作用在迄今为止测试的所有物种中都存在，人类可能也不例外。预计随着预处理机制被更深入地理解，药物预处理将在临床上得到实际应用。
