Lamendola Priscilla, Di Monaco Antonio, Barone Lucy, Pisanello Chiara, Lanza Gaetano A, Crea Filippo
Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma
G Ital Cardiol (Rome). 2009 Jan;10(1):28-36.
Myocardial cell damage caused by myocardial ischemia results from several factors that include the duration of ischemia, oxygen demand by cardiomyocytes at the time of ischemia, and the presence and entity of collateral blood flow to the ischemic area. Importantly, myocardial cell injury may derive not only from ischemia itself but also from detrimental phenomena occurring during the restoration of myocardial blood flow after the ischemic episode (reperfusion damage). In the last decades a lot of studies have demonstrated that cardiomyocytes have several mechanisms that provide them protection against the damage deriving from ischemia-reperfusion, also allowing a prolongation of survival in the most severe cases. In this article we review some of these mechanisms, also discussing their present and/or potential therapeutic applications in the clinical setting. The topics include the interventions aimed at reducing cardiac work through a reduction of oxygen demand by myocardial cells or at optimizing the utilization of energetic resources by myocardial cells in situations of ischemia, the importance of phenomena such as ischemic preconditioning (early and delayed) and postconditioning of myocardial cells, and, finally, the theoretic possibility of interventions aimed at preventing cell death consequent to apoptosis.
心肌缺血所致的心肌细胞损伤源于多种因素,包括缺血持续时间、缺血时心肌细胞的需氧量以及缺血区域侧支血流的存在与否及情况。重要的是,心肌细胞损伤不仅可能源于缺血本身,还可能源于缺血发作后心肌血流恢复期间发生的有害现象(再灌注损伤)。在过去几十年中,许多研究表明心肌细胞具有多种机制,可保护它们免受缺血 - 再灌注损伤,在最严重的情况下还能延长存活时间。在本文中,我们回顾其中一些机制,并讨论它们在临床环境中的当前和/或潜在治疗应用。主题包括旨在通过降低心肌细胞需氧量来减少心脏工作的干预措施,或在缺血情况下优化心肌细胞能量资源利用的干预措施,心肌细胞缺血预处理(早期和延迟)和后处理等现象的重要性,以及最后,旨在预防因凋亡导致细胞死亡的干预措施的理论可能性。