Mechanisms of ventricular arrhythmias during myocardial ishemia and reperfusion

在模拟低氧条件下，对豚鼠单个心肌细胞的电活动和机械活动进行了研究。同时记录肌节的局部运动和膜电位，并用微型计算机图像处理系统进行分析。暴露于5 mM CN^可引起动作电位时程进行性缩短和抽动收缩减弱。CN处理后约30~70min，心肌细胞不再兴奋。去除CN^-后，心肌细胞从-95 mV的静息电位水平呈现周期性的微型膜去极化。微小的去极化在2-5分钟内频率和幅度增加，并在某些情况下诱发自发动作电位。当去极化幅度小于5 mV，持续时间大于500毫秒时，伴有局限性的肌节缩短，类似于传播的收缩波(单灶性振荡)。更大幅度和更短持续时间的膜去极化与更均匀的局部肌节缩短(多焦振荡法)相关。这种电和机械振荡逐渐减弱，并在6-8分钟内消失。在冲洗期施加的一连串电刺激引起电位波动的一过性增大和肌节缩短的同步性增强。这些结果表明，氧化磷酸化恢复时细胞内钙离子浓度的不均匀升高可能引起膜电位的振荡波动，从而导致异常的自发兴奋。

Electrical and mechanical activities of guinea pig single ventricular myocytes were investigated under conditions simulating hypoxiareoxygenation. The localized movement of sarcomere was recorded simultaneously with membrane potential, and analyzed using a microcomputerbased image processing system. Exposure to 5 mM CN^- caused progressive shortening of action potential duration and attenuation of twitch contraction. The myocytes became inexcitable about 30 to 70 min after the CN^- treatment. On removal of CN^-, the myocytes exhibited periodic miniature membrane depolarizations from the resting potential level of -95 mV. The miniature depolarizations increased in frequency and in amplitude within 2-5 min and, in some cases, spontaneous action potentials were induced. When depolarizations were smaller than 5 mV in amplitude and longer than 500 msec in duration, they were accompanied by localized sarcomere shortening like a propagating contractile wave (unifocal oscillation). Membrane depolarizations of larger amplitude and shorter duration were associated with a more uniform pattern of localized sarcomere shortening (multifocal ocsillation). Such electrical and mechanical oscillations were attenuated gradually and disappeared within 6-8 min. Trains of electrical stimuli applied during the washing out period caused transient augmentation of potential fluctuation and enhancement of synchronization of sarcomere shortening. These results suggest that nonuniform elevation of intracellular calcium concentration at the resumption of oxidative phosphorylation may initiate oscillatory fluctuations of membrane potential leading to abnormal spontaneous excitation.