Arutunyan Ara, Swift Luther M, Sarvazyan Narine
Department of Physiology, Health Sciences Center, Texas Tech University, 3601 Fourth Street, Lubbock, TX 79430, USA.
Am J Physiol Heart Circ Physiol. 2002 Aug;283(2):H741-9. doi: 10.1152/ajpheart.00096.2002.
The objective of the present study was to directly visualize ectopic activity associated with ischemia-reperfusion and its progression to arrhythmia. To accomplish this goal, we employed a two-dimensional network of neonatal rat cardiomyocytes and a recently developed model of localized ischemia-reperfusion. Washout of the ischemia-like solution resulted in tachyarrhythmic episodes lasting 15-200 s. These episodes were preceded by the appearance of multiple ectopic sources and propagation of ectopic activity along the border of the former ischemic zone. The ectopic sources exhibited a slow rise in diastolic calcium, which disappeared upon return to the original pacing pattern. Border zone propagation of ectopic activity was followed by its escape into the surrounding control network, generating arrhythmias. Together, these observations suggest that upon reperfusion, a distinct layer, which consists of ectopically active, poorly coupled cells, is formed transiently over an injured area. Despite being neighbored by a conductive and excitable tissue, this transient functional layer is capable of sustaining autonomous waves and serving as a special conductive medium through which ectopic activity can propagate before spreading into the surrounding healthy tissue.
本研究的目的是直接观察与缺血再灌注相关的异位活动及其向心律失常的进展。为实现这一目标，我们采用了新生大鼠心肌细胞的二维网络和最近开发的局部缺血再灌注模型。冲洗类似缺血的溶液导致持续15 - 200秒的快速心律失常发作。这些发作之前会出现多个异位起搏点，并沿先前缺血区的边界传播异位活动。异位起搏点的舒张期钙缓慢升高，恢复到原始起搏模式后消失。异位活动在边界区传播后，会逸入周围的对照网络，引发心律失常。这些观察结果共同表明，再灌注时，在损伤区域会短暂形成一个由异位活跃、耦合不良的细胞组成的独特层。尽管与传导性和兴奋性组织相邻，但这个短暂的功能层能够维持自主波，并作为一种特殊的传导介质，使异位活动在扩散到周围健康组织之前得以传播。
