MECHANISMS OF ABNORMAL AUTOMATICITY IN CARDIAC PREPARATIONS

虽然静息的哺乳动物心室肌通常不表现出 起搏器样活动，在某些条件下自发局部 肌浆网（SR）释放Ca 2+导致 肌浆[Ca 2 +]（Ca-i），其引起微小的内向电流， 在膜电位的振荡中。 在正常的静息膜上 心肌细胞的电位不足以引起动作 潜力 然而，当自发SR Ca 2+释放同时发生时， 在多于一个基因座处，即当这些基因座“同步化”时， 所产生的肌膜去极化增加到 有时足以产生自发动作电位， 收缩。 因此，多个区域的局部自发性Ca 2+释放 在心室心肌细胞内，如果“同步”是一种机制， 这些细胞中的异常自律性，可以产生“心脏跳动， 反面. "

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."