Downey J M, Cohen M V
Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688, USA.
Adv Exp Med Biol. 1997;430:39-55. doi: 10.1007/978-1-4615-5959-7_4.
Ischemic preconditioning is a phenomenon in which exposure of the heart to a brief period of ischemia causes it to quickly adapt itself to become resistant to infarction from a subsequent ischemic insult. The mechanism is not fully understood but, at least in the rabbit, it is known to be triggered by occupation of adenosine receptors, opioid receptors, bradykinin receptors and the generation of free radicals during the preconditioning ischemia. All of these are thought to converge on and activate protein kinase C (PKC), which in turn activates a tyrosine kinase. This kinase cascade eventually terminates on some unknown effector, possibly a potassium channel or a cytoskeletal protein, which makes the cells resistant to infarction. If this process can be understood, it should be possible to devise a method for conferring this protection to patients with acute myocardial infarction.
缺血预处理是一种现象，即心脏短暂暴露于缺血状态会使其迅速适应，从而对随后的缺血性损伤产生梗死抗性。其机制尚未完全明确，但至少在兔子中，已知它是由预处理缺血期间腺苷受体、阿片受体、缓激肽受体的占据以及自由基的产生所触发的。所有这些都被认为会汇聚并激活蛋白激酶C（PKC），而蛋白激酶C又会激活一种酪氨酸激酶。这种激酶级联反应最终作用于一些未知的效应器，可能是一种钾通道或一种细胞骨架蛋白，从而使细胞具有梗死抗性。如果能够理解这个过程，就应该有可能设计出一种方法，为急性心肌梗死患者提供这种保护。
