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关于保护缺血心肌的研究,七十年代以前主要在调节心肌血氧的供需平衡,强调降低心脏负荷,增加冠状动脉血流量和促进侧枝循环的建立等。八十年代以来,对心肌缺血损伤发病机理的认识深入到细胞分子水平,研究重点转到了细胞保护。所谓细胞保护(Cytoprotection)的概念,是指增强心肌细胞对缺血、缺氧等损伤的抵抗力(耐受性),阻止细胞损伤向不可逆方向发展,提高细胞的存活率。目前已知,恢复缺血心肌的供血,供氧并不一定能挽救已受缺血损伤的细胞,有时甚至还加速细胞向不可逆损伤发展(即再灌注反常、氧反常等现象)。基于对缺血再灌注(I/R)损伤发病机理的认识,目前对缺血心肌细胞保护常用的实验治疗有以下几种措施: 1.调节细胞内Ca~(2+)稳态。细胞内钙超载(Ca overload)是细胞不可逆损伤的共同通路。I/R损伤时心肌细胞内Ca~(2+)聚积的机制非常复杂,Ca~(2+)内流的增
On the protection of ischemic myocardium, before the seventies mainly in the regulation of myocardial oxygen supply and demand balance, emphasizing the reduction of cardiac load, increase coronary blood flow and promote the establishment of collateral circulation. Since the 1980s, the understanding of the pathogenesis of myocardial ischemic injury has deepened into the molecular level of cells, and the focus of research has shifted to cytoprotection. The so-called cytoprotection concept, refers to enhance the myocardial cells of ischemia, hypoxia and other damage resistance (tolerance), to prevent cell damage to the irreversible direction, improve cell survival rate. It is known that restoration of blood supply to ischemic myocardium does not necessarily save cells that have been damaged by ischemia, and sometimes accelerates the development of cells to irreversible damage (ie, reperfusion abnormalities and oxygen abnormalities). Based on the understanding of the pathogenesis of ischemia / reperfusion (I / R) injury, the current experimental methods for the protection of ischemic cardiomyocytes are as follows: 1. Regulate intracellular Ca ~ (2+) homeostasis. Intracellular calcium overload is the common pathway of irreversible cell damage. The mechanism of intracellular accumulation of Ca ~ (2+) in I / R injury is very complex. The mechanism of Ca ~ (2+) influx