Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
Int J Surg. 2009 Dec;7(6):490-8. doi: 10.1016/j.ijsu.2009.06.004. Epub 2009 Jun 21.
Ischemia/reperfusion (I/R) injury is a major contributory factor to cardiac dysfunction and infarct size that determines patient prognosis after acute myocardial infarction. During the last 20 years, since the appearance of the first publication on ischemic preconditioning (IP), our knowledge of this phenomenon has increased exponentially.
Basic scientific experiments and preliminary clinical trials in humans suggest that IP confers resistance to subsequent sustained ischemic insults not only in the regional tissue but also in distant organs (remote ischemic preconditioning), which may provide a simple, cost-effective means of reducing the risk of perioperative myocardial ischemia. The mechanism may be humoral, neural, or a combination of both, and involves adenosine, bradykinin, protein kinases and K(ATP) channels, although the precise end-effector remains unclear. This review describes different signaling pathways involved in acute ischemic preconditioning in detail.
缺血/再灌注（I/R）损伤是导致心功能障碍和梗死面积的主要因素，决定了急性心肌梗死后患者的预后。在过去的 20 年中，自第一篇关于缺血预处理（IP）的出版物出现以来，我们对这一现象的认识呈指数级增长。
基础科学实验和初步的人体临床试验表明，IP 不仅在区域性组织中，而且在远处器官（远程缺血预处理）中赋予对随后持续缺血性损伤的抗性，这可能提供一种简单、经济有效的方法来降低围手术期心肌缺血的风险。其机制可能是体液的、神经的或两者的结合，涉及腺苷、缓激肽、蛋白激酶和 KATP 通道，尽管确切的终末效应器尚不清楚。这篇综述详细描述了急性缺血预处理中涉及的不同信号通路。
