Kamiyama A, Eguchi K, Shibayama R
Jpn Circ J. 1986 Jan;50(1):65-73. doi: 10.1253/jcj.50.65.
Mechanisms of ventricular tachycardia induced by local application of a properly timed premature stimulus were studied with routine microelectrode technique and extracellular recordings on a ventricular sheet. Thinly sliced preparations obtained from subepicardial muscle of the canine ventricle were used as an approximation of a two-dimensional model. On these preparations, spontaneously sustained tachycardia easily induced by a single premature stimulus. Since delayed after-depolarizations were never evoked by frequent stimulations even in the K+-free and high-Ca++ media, these tachycardias seemed to be induced by re-entrant and circus movement mechanisms. To analyse the re-entrant mechanisms, action potentials generated by normal driving stimuli were recorded from multiple points (40 approximately 50 points) and the spreads of the depolarization and repolarization phases of the action potentials were mapped. The depolarizing wave front on the map always showed a circular or elliptical pattern. Whenever the pattern of spread of the repolarizing wave was similar to that of the depolarizing wave, sustained tachycardia was never brought about by any premature stimulus. On the other hand, when the map of the spread of the repolarizing wave was very complicated and mixed with that of the depolarizing wave, sustained tachycardia was frequently induced. From the above results, it is suggested that the nonuniform recovery of excitability plays a role in the generation of sustained tachycardia. Moreover, a portion of the unidirectional block of the premature impulse was determined by calculated using the conduction velocity of the premature impulse and the effective refractory period in each cell; then a route of re-entry for the premature impulse was simulated.(ABSTRACT TRUNCATED AT 250 WORDS)
采用常规微电极技术和细胞外记录方法,在心室肌薄片上研究了适时施加单个期前刺激诱发室性心动过速的机制。取自犬心室心外膜下肌肉的薄片标本被用作二维模型的近似物。在这些标本上,单个期前刺激很容易诱发自发持续性心动过速。由于即使在无钾和高钙培养基中频繁刺激也从未诱发延迟后去极化,这些心动过速似乎是由折返和环形运动机制诱发的。为了分析折返机制,从多个点(约40至50个点)记录正常驱动刺激产生的动作电位,并绘制动作电位去极化和复极化阶段的传播图。图上去极化波前总是呈现圆形或椭圆形模式。每当复极化波的传播模式与去极化波相似时,任何期前刺激都不会引发持续性心动过速。另一方面,当复极化波传播图非常复杂且与去极化波传播图混合时,频繁诱发持续性心动过速。根据上述结果,提示兴奋性恢复不均一在持续性心动过速的发生中起作用。此外,通过计算期前冲动的传导速度和每个细胞的有效不应期来确定期前冲动单向阻滞的一部分;然后模拟期前冲动的折返途径。(摘要截短于250字)