Mechanisms of ventricular arrhythmias during myocardial ishemia and reperfusion

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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.