MECHANISMS OF ABNORMAL AUTOMATICITY IN CARDIAC PREPARATIONS

休息时哺乳动物心室肌通常不会表现出 类似起搏器的活动，在某些条件下自发的局部活动 肌浆网 (SR) 释放 Ca2 导致 肌质 [Ca2 ] (Ca-i) 导致微型内向电流 在膜电位的振荡中。 在正常的静息膜处 心肌细胞的潜力不足以诱导作用 潜力。 然而，当自发 SR Ca2 释放同时发生时 在多个基因座上，即当这些基因座“同步”时， 由此产生的肌膜去极化增强至以下水平 有时足以产生自发动作电位并且 收缩。 因此，局部自发 Ca2 释放的多个区域 在心室心肌细胞内，如果“同步”是一种机制 这些细胞异常的自动化，可以产生“心跳” 逆转。”

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."