In situ visualization of the intracellular Ca2+ dynamics at the border of the acute myocardial infarct

缺血边界区心肌[Ca^<2+>]_1动力学异常可引起急性心肌梗死的各种并发症，但其细胞方面仍不确定。在冠脉闭塞2小时时，观察灌注氟3/AM的大鼠心肌梗死心外膜边界区（EBZ）的实时共焦[Ca^<2+>]_1动态。电离层无均匀的Ca^<2+>瞬态。相反，两种类型的细胞内Ca^<2+>波出现在两个不同的区域；毗邻地区毗邻。梗死边缘及其周围。相邻区域的Ca^<2+>波（n=78）在相邻区域出现的频率（17.6 ^^+__- 10.7波/min/细胞）和细胞内传播速度（198.4 ^^+__- 42.6 um/s）比在可见区域（7.1 ^^+__- 4.6波/min/细胞和140.8 ^^+__- 31.2 um/s）更高（n=76）。在时间推移分析中，这些参数依次下降，相邻区域的下降速度快于附近区域。随着波的消失，静止肌细胞呈斑片状分布，既没有出现[Ca^<2+>]_1波动，也没有出现高静态[Ca^<2+>]_1波动。异丙肾上腺素逆转了邻近区域的连续下降，而不是邻近区域。琥珀酸脱氢酶（反映线粒体ATP的产生）的组织化学表明与[Ca^<2+>]_1动力学的空间不均匀性密切相关。这些数据首次提供了急性心肌梗死EBZ内异常[Ca^<2+>]_1动力学的细胞方面。由[Ca^<2+>]_1负荷和代谢条件决定的Ca^<2+>波和静止肌细胞的不均匀分布将导致急性心肌梗死期间发生的机电功能障碍

Although abnormal [Ca^<2+>]_1 dynamics at ischemic border zone myocardium causes various complications in acute myocardial infarction, its cellular aspects remain uncertain. Real-time confocal [Ca^<2+>]_1 dynamics were visualized at epicardial border zones (EBZ) of rat myocardial infarcts loaded with fluo 3/AM under 2-hr coronary occlusion. EBZ exhibited no spatially homogeneous Ca^<2+> transients. Instead, two types of intracellular Ca^<2+> waves emerged at two different regions; the adjacent region adjoining. The infarctedmargin and its surrounding vicinity. The waves at the vicinity emerged synchronously upon Ca^<2+> transients, whereas those at the adjacent region arose independently of ventricular exsitation Ca^<2+> waves (n=78) at the adjacent regions exhibited more frequently (17.6 ^^+__- 10.7 waves/min/cell) and with more rapid intracellular propagation (the propagation velocity was 198.4 ^^+__- 42.6 um/s) than those (n=76) at the visinity (7.1 ^^+__- 4.6 waves/min/cell and 140.8 ^^+__- 31.2 um/s, respectively). On time-lapse analysis these parameters decreased sequenially with quicker decline at the adjacent regions than at the vicinities. The accompanying disappearance of the waves resulted in patchy distribution of quiescent myocytes showing neither [Ca^<2+>]_1 fluctuations nor high-static [Ca^<2+>]_1. Isoproterenol reversed the sequential decline at the vicinities but not at the adjacent regions. Histochemistry for succinate dehydrogenase (reflecting mitochondrial ATP production) indicated close relevance to the spatial inhomogeneity of [Ca^<2+>]_1 dynamics. These data are the first to provide cellular aspects of abnormal [Ca^<2+>]_1 dynamics within EBZ of acute myocardial infarct. The inhomogeneous distribution of Ca^<2+> waves and quiescent myocytes, determined by both [Ca^<2+>]_1 loading and metabolic conditions, would contribute to electromechanical dysfunction that occur during acute myocardial infarction