MECHANISMS OF ABNORMAL AUTOMATICITY IN CARDIAC PREPARATIONS

而静息的哺乳动物心肌通常不会表现出 起搏样活动，在一定条件下自发局部化 肌浆网(SR)释放钙导致血管紧张素转换酶活性增加 引起微小内向电流的肌浆[Ca-i](Ca-i) 在膜电位的振荡中。在正常的静息膜上 在心肌细胞中的电位这不足以引起一种动作 潜力。然而，当自发性肌质网钙释放同时发生时 在多个基因座，即当这些基因座“同步”时， 由此产生的肌膜去极化增强到 有时足以产生自发的动作电位 收缩。因此，多个区域的局部自发钙释放 在心肌细胞内，如果“同步化”是一种 在这些细胞中存在异常的自律性，并会产生“心跳加速” 颠倒过来。“

While resting mammalian ventricular myocardium does not usually exhibit pacemaker like activity, under certain conditions spontaneous localized release of Ca2+ from sarcoplasmic reticulum (SR) results in an increase in myoplasmic [Ca2+] (Ca-i) which causes miniature inward currents resulting in oscillations of membrane potential. At the normal resting membrane potential in cardiac myocytes this is insufficient to induce an action potential. However, when spontaneous SR Ca2+ release occurs simultaneously at more than a single locus, i.e. when these loci are "synchronized," the resultant sarcolemmal depolarization is augmented to levels that are sometimes sufficient to produce a spontaneous action potential and contraction. Thus, multiple areas of localized spontaneous Ca2+ release within ventricular cardiac cells, if "synchronized" is a mechanism for abnormal automaticity in these cells and can produce a "heart beat in reverse."