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Mechanisms of ventricular arrhythmias during myocardial ishemia and reperfusion

心肌缺血再灌注时室性心律失常的机制

基本信息

批准号：
61480206
负责人：
TOYAMA Junji
金额：
$ 2.88万
依托单位：
Department of Circulation and Respiration, The Research Institute of Environmental Medicine, Nagoya, University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1987
项目状态：
已结题

项目摘要

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.

在模拟缺氧复氧的条件下研究了豚鼠单心室肌细胞的电和机械活动。肌节的局部运动与膜电位同时记录，并使用基于微计算机的图像处理系统进行分析。暴露于 5 mM CN^- 导致动作电位持续时间逐渐缩短和抽搐收缩减弱。 CN 2- 处理后约30至70分钟，肌细胞变得不兴奋。去除 CN^- 后，肌细胞表现出从 -95 mV 静息电位水平周期性的微型膜去极化。微型去极化的频率和幅度在 2-5 分钟内增加，并且在某些情况下，诱导自发动作电位。当去极化幅度小于 5 mV 且持续时间长于 500 毫秒时，它们会伴随着局部肌节缩短，就像传播的收缩波（单焦点振荡）。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模式（多焦点振荡）相关。这种电气和机械振荡逐渐减弱并在6-8分钟内消失。在清洗期间施加的一系列电刺激引起电位波动的瞬时增强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浓度的不均匀升高可能引发膜电位的振荡波动，导致异常的自发兴奋。