Gough W B, Zeiler R H, El-Sherif N
Am J Cardiol. 1984 Jan 15;53(2):303-6. doi: 10.1016/0002-9149(84)90443-0.
Triggered activity arising from a delayed afterdepolarization occurs in canine subendocardial Purkinje fibers 1 day after myocardial infarction (MI). Standard microelectrode techniques were used to study small preparations (20 to 48 mm2) in vitro. Nifedipine, 1 mg/liter, reversibly suppressed triggered activity by reducing maximum diastolic potential, action potential amplitude and the rate of depolarization of the delayed afterdepolarization. Complete quiescence or exit block resulted. The effects of nifedipine were antagonized by elevating extracellular calcium ion concentration. These results suggest that spontaneous ectopic rhythms 1 day after MI that are the result of triggered activity are dependent on transmembrane calcium ion movement, which nifedipine can directly antagonize.
延迟后去极化引发的触发活动发生在犬心肌梗死(MI)后1天的心内膜下浦肯野纤维中。采用标准微电极技术在体外研究小组织标本(20至48平方毫米)。1毫克/升的硝苯地平通过降低最大舒张电位、动作电位幅度和延迟后去极化的去极化速率,可逆地抑制触发活动。导致完全静止或传出阻滞。升高细胞外钙离子浓度可拮抗硝苯地平的作用。这些结果表明,MI后1天由触发活动导致的自发性异位节律依赖于跨膜钙离子移动,而硝苯地平可直接拮抗这种移动。