Evrengul Harun, Seleci Deniz, Tanriverdi Halil, Kaftan Asuman
Department of Cardiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey.
Coron Artery Dis. 2006 May;17(3):283-8. doi: 10.1097/00019501-200605000-00013.
Potentially hazardous short ischemic episodes increase the tolerance of myocardium to ischemia paradoxically. This condition decreases the infarct area markedly caused by a longer duration of coronary occlusion. This phenomenon is known as 'ischemic preconditioning' and its powerful cardioprotective effect has been shown in experimental and clinical studies. Ischemic preconditioning decreases cardiac mortality markedly by preventing the development of left ventricular dysfunction and ventricular and supraventricular arrhythmias after acute myocardial infarction. Ischemia-induced opening of ATP-sensitive potassium channels and synthesis of stress proteins via activation of adenosine, bradykinin and prostaglandin receptors seem to be the possible mechanisms. By understanding the underlying mechanisms of ischemic preconditioning, it may be possible to develop new pharmacologic agents that cause ischemic preconditioning with antiischemic and antiarrhythmic properties without causing myocardial ischemia.
潜在危险的短暂缺血发作会反常地增加心肌对缺血的耐受性。这种情况会显著减少由较长时间冠状动脉闭塞所导致的梗死面积。这种现象被称为“缺血预处理”,其强大的心脏保护作用已在实验和临床研究中得到证实。缺血预处理通过预防急性心肌梗死后左心室功能障碍以及室性和室上性心律失常的发生,显著降低心脏死亡率。缺血诱导ATP敏感性钾通道开放以及通过激活腺苷、缓激肽和前列腺素受体合成应激蛋白似乎是可能的机制。通过了解缺血预处理的潜在机制,有可能开发出具有抗缺血和抗心律失常特性且不会导致心肌缺血的新型药物,从而引发缺血预处理。