Mechanisms of ventricular arrhythmias during myocardial ishemia and reperfusion

本文研究了豚鼠单个心室肌细胞在模拟缺氧复氧条件下的电活动和机械活动。肌节的局部运动与膜电位同步记录，并用微机图像处理系统进行分析。暴露于5 mM CN^-可导致动作电位时程进行性缩短和抽搐收缩减弱。CN-处理后约30至70分钟，心肌细胞变得不可兴奋。去除CN^-后，心肌细胞表现出周期性的微小膜去极化，静息电位水平为-95 mV。在2-5分钟内，微型去极化的频率和幅度增加，在某些情况下，诱发自发动作电位。当去极化幅度小于5 mV，持续时间长于500 msec时，它们伴随着局部肌节缩短，如传播的收缩波（单焦振荡）。较大幅度和较短持续时间的膜去极化与更均匀的局部肌节缩短模式（多灶性颤动）相关。这种电和机械振荡逐渐减弱，并在6-8分钟内消失。在冲洗期间施加的电刺激列车引起的电位波动和肌节缩短的同步性增强的瞬时增强。这些结果表明，细胞内钙离子浓度的不均匀升高在氧化磷酸化的恢复可能会引发振荡波动的膜电位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.