Alkhulaifi A M, Jenkins D P, Pugsley W B, Treasure T
Harefield Hospital, Middlesex, UK.
Eur J Cardiothorac Surg. 1996;10(9):792-8. doi: 10.1016/s1010-7940(96)80342-3.
This review discusses the phenomenon of ischaemic preconditioning and its potential application to cardiac surgery. The biology of ischaemic preconditioning is explained and the more limited evidence suggesting that the human heart can be preconditioned is discussed.
It is now accepted that the heart is capable of short-term rapid adaptation in response to brief ischaemia so that during a subsequent, more severe ischaemic insult myocardial necrosis is delayed-ischaemic preconditioning. The infarct-delaying properties of ischaemic preconditioning have been observed in all species studied. Five minutes of ischaemia is enough to initiate preconditioning and the protective period lasts for 1-2 h. Laboratory experiments have demonstrated that the stimulation of adenosine receptors initiates preconditioning and the intracellular signal transduction mechanisms involve protein kinase C and ATP-dependent potassium channels, although there may be some differences between species. An analysis of studies on myocardial infarction in humans has revealed that some patients reporting angina in the days before infarction have a better outcome and this may be due to the ischaemia causing preconditioning. More direct evidence has come from an investigation of patients undergoing percutaneous transluminal angioplasty in whom the ST-segment changes induced by balloon inflation were more marked during the first inflation than the second. In patients undergoing coronary artery bypass grafting the decline in ATP content during the first 10 min of ischaemia was reduced in patients subjected to a brief preconditioning protocol.
Preconditioning is a powerful and reproducible method of protecting the myocardium from irreversible ischaemic injury. There is now evidence indicating that the human heart can be preconditioned. However, more trials are necessary in patients undergoing cardiac surgery before the role of preconditioning as a means of myocardial protection can be assessed.
本综述讨论缺血预处理现象及其在心脏手术中的潜在应用。解释了缺血预处理的生物学机制，并探讨了关于人类心脏可进行预处理的较为有限的证据。
现在人们公认，心脏能够对短暂缺血做出短期快速适应，从而在随后更严重的缺血性损伤中延迟心肌坏死，即缺血预处理。在所有研究的物种中均观察到了缺血预处理的梗死延迟特性。五分钟的缺血足以启动预处理，保护期持续1 - 2小时。实验室实验表明，腺苷受体的刺激启动预处理，细胞内信号转导机制涉及蛋白激酶C和ATP依赖性钾通道，尽管不同物种之间可能存在一些差异。对人类心肌梗死研究的分析表明，一些在梗死前几天报告有心绞痛的患者预后较好，这可能是由于缺血导致了预处理。更直接的证据来自对接受经皮腔内血管成形术患者的调查，其中球囊扩张引起的ST段变化在第一次扩张时比第二次更明显。在接受冠状动脉旁路移植术的患者中，采用简短预处理方案的患者在缺血最初10分钟内ATP含量的下降有所减少。
预处理是一种强大且可重复的保护心肌免受不可逆缺血损伤的方法。现在有证据表明人类心脏可以进行预处理。然而，在能够评估预处理作为心肌保护手段的作用之前，需要对接受心脏手术的患者进行更多试验。
