MECHANISMS OF ABNORMAL AUTOMATICITY IN CARDIAC PREPARATIONS

而静息的哺乳动物心室肌通常 在某些条件下表现出类似起搏器的活动 肌浆自发性局部Ca ~（2+）释放 内质网（SR）导致肌浆（Ca 2+）（Cai）增加 从而产生微小的内向电流， 膜电位 在正常的静息膜电位下 在心肌细胞中，这不足以诱导作用 潜力 然而，当自发SR Ca 2+释放发生时， 同时在一个以上的位点，即当这些位点 是“同步的”，所产生的肌膜去极化是 增加到有时足以产生 自发动作电位和收缩。 因此， 心室内局部自发性钙释放面积 心脏细胞，如果“同步”是一种机制， 在这些细胞中的自动性，并可以产生“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+) (Cai) which cause 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."