The study of the mechanism and characteristics of triggered-activity

触发活动是心律失常发生的重要细胞因素之一。产生触发活性的膜电位变化是由几种不同的机制引起的，具体取决于实验条件。为了阐明这些电位变化的本质和离子机制，本实验对狗、豚鼠、兔和蛙的心肌细胞进行了单蔗糖间隙或全细胞钳制的微电极技术和电压钳技术。在&lt；Ca^(2+)&gt；-过载条件下，暴露于低&lt；K^+&gt；，高&lt；Ca^(2+)&gt；溶液中，触发活动是由瞬时内向电流形成的延迟后除极引起的。根据对电刺激的反应，以及它们的电压和时间依赖性，充分分析了这些延迟后去极化和瞬时内向电流的特征。这些信息可作为基于这些…的临床心律失常的诊断线索更多的活动，但不同于再入或自动。研究还揭示，瞬时内向电流不仅在复极时被激活，而且在去极化电压下也被激活，反映了肌浆网中~lt；Ca^(2+)&gt；的周期性释放。用&lt；Ca^(2+)&gt；阻断剂证实了通过慢通道的&lt；Ca^(2+)&gt；内流对激活瞬时内向电流的贡献，其对触发的心律失常的作用可通过抑制&lt；Ca^(2+)&gt；电流来解释。电缆分析表明，在延迟后去极化和触发活动的发展过程中，内部纵向电阻增加。研究表明，Ba2+诱发的延迟后去极化和自律性不是由瞬时内向电流的激活引起的，而是由内向整流电流&lt；K^+&gt；作用引起的。&lt；Ba^(2+)&gt；产生时间和电压依赖的阻断，导致延迟后除极和自律性。乌头碱是另一种产生延迟后除极和触发活动的药物。在这种情况下，由乌头碱负载~lt；Na~+&gt；触发的瞬时内向电流是一个促成因素。因此，触发活动不是由单一的离子机制引起的，而是由几种不同的机制引起的，这可能解释了这些心律失常的复杂性质。较少

Triggered-activity is one of important cellular factors for the genesis of arrhythmias. The membrane potential changes to produce triggered-activity are brought by several different mechanisms depending on the experimental conditions. To clarify the nature and the ionic mechanism of these potential changes, the microelectrode technique and voltage clamp method of the single sucrose gap or whole-cell clamp were applied to heart cells from dog, guinea pig, rabbit and frog. In the <Ca^(2+)> -overloaded conditions by exposing to the low <K^+> , high <Ca^(2+)> solutions, triggered-activity was caused by delayed afterdepolarization which was formed by the transient inward current. The characteristics of these delayed afterdepolarizations and the transient inward current were fully analyzed in terms of the responses to the electrical stimulation, as well as their voltage and time dependent natures. These informations may be used as diagnostic clues for the clinical arrhythmias based on these … More activities but different from reentry or automaticity. The study also disclosed that the transient inward current was activated not only upon repolarization but also during the depolarizing voltages, reflecting cyclic release of <Ca^(2+)> from the sarcoplasmic reticulum. The contribution of <Ca^(2+)> influx via the slow channel to the activation of the transient inward current was demonstrated by use of the <Ca^(2+)> blockers and their actions on triggered-arrhythmias can be explained by the inhibition of the <Ca^(2+)> current. The increase in the internal longitudinal resistance during the development of the delayed afterdepolarizations and triggered-activity was demonstrated by the cable analysis. The study demonstrated that the barium-induced delayed afterdepolarization and automaticity were not brought by the activation of the transient inward current, but by the <Ba^(2+)> action on the inward rectifier <K^+> current ( <I_(kl)> ). <Ba^(2+)> produced time- and voltage-dependent blockade of <I_(kl)> , which induced the delayed afterdepolarizations and automaticity. Aconitine is another agent to produce delayed afterdepolarizations and triggered-activity. In this case, the transient inward current which was triggered by the <Na^+> loading by aconitine, was shown to be a contributing factor. Therefore, triggered-activity is brought not by a single ionic mechanism, but by several different mechanisms, which may explain complex natures of these arrhythmias. Less