Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle.
Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle.
复制标题
兔心房肌的马戏团运动作为心动过速的机制。
作者：
A. Maurits;Allessie;M. FélixI;Bonke;G. FRANCIENJ.;Schopman
摘要在兔心房心肌的小块中，通过诱导一个适当定时的过早脉冲产生持续时间的环形运动心动过速。通过使用多个细胞内和细胞外电极，可以准确地分析心动过速期间激活的传播。因为在目前的实验中，冲动在周围循环没有明显的解剖学障碍，我们特别注意发生在马戏团运动中心的现象。我们发现，在一个不可兴奋的中央障碍的情况下，马戏团运动的中心被多个向心小波侵入，这些小波聚集在电路的中心。在这些观察的基础上，我们开发了一个新的模型循环兴奋的心脏组织。该模型的属性（被称为“领先的圆圈概念”）进行了比较，与周围的解剖障碍马戏团运动的行为。结果表明，这两种类型的马戏运动心动过速的反应不同的基本电生理特性的变化，如传导速度和不应期。例如，在组织浴中加入氨甲酰胆碱可引起前环心动过速的明显加速，而心房组织环中的环运动几乎不受影响。另一方面，抑郁症的传导速度暴露于中等浓度的河豚毒素有一个更明显的影响，马戏团运动的环准备比心动过速的基础上领先的循环机制。最后，我们建议使用的强度-间期曲线-经过一些修改-来描述和预测的行为，一个领先的环心动过速。在我们关于家兔心房肌的环状运动的系列论文中，我们能够证明，在一小块心房肌中，适当定时的早搏的诱导可以迫使冲动以迂回的路线传导，从而为心动过速的一段时间做好准备。我们收集的证据表明，心房中自然存在的兴奋性不均匀恢复对于过早冲动的单向阻滞的发生至关重要，当然，这是马戏运动开始的先决条件。此外，通过使用同步多微电极记录的技术，我们获得了有关细胞反应的详细信息，在启动的马戏团运动。[2]然而，到目前为止，在没有解剖学障碍的情况下，还没有得出马戏团运动的结论性模型。这主要是由于缺乏关于循环脉冲中心发生了什么的信息。在大多数关于马戏团运动和再入的研究中，使用了1913年由Mines 3引入的模型。该模型基于对心脏组织环形条带的观察，并隐含地假设存在某种总体解剖障碍。但在
SUMMARY In small pieces of rabbit atrial myocardium, sustained periods of circus movement tachycardia were produced by the induction of a single properly timed premature impulse. By use of multiple intracellular and extracellular electrodes the spread of activation during the tachycardia could be analyzed accurately. Because in the present experiments there was no gross anatomical obstacle for the impulse to circulate around, we paid special attention to phenomena occurring in the center of the circus movement. We found that in the absence of an inexcitable central obstacle the center of a circus movement was invaded by multiple centripetal wavelets which converged in the very center of the circuit. On the basis of these observations we developed a new model of circulating excitation in cardiac tissue. The properties of this model (referred to as the "leading circle concept") were compared with the behavior of circus movement around the anatomical obstacle. It turned out that both types of circus movement tachycardia responded differently to changes in basic electrophysiological properties such as conduction velocity and refractory period. For example, addition of carbamylcholine to the tissue bath caused a marked acceleration of the leading circle tachycardia, whereas circus movement in a ring of atrial tissue was hardly affected. On the other hand, depression of conduction velocity by exposure to moderate concentrations of tetrodotoxin had a more pronounced effect on circus movement in the ring preparations than on tachycardias based on a leading circle mechanism. Finally we suggest the use of the strength-interval curve —after some modification —to describe and predict the behavior of a leading circle tachycardia. IN OUR SERIES of papers on circus movement in rabbit atrial muscle 1 ' 2 we were able to show that in a small piece of atrial myocardium the induction of a properly timed premature beat can force the impulse to conduct in a circuitous route and thus set the stage for a period of tachycardia. We gathered evidence that the naturally existing nonuniform recovery of excitability in the atrium was of major importance for the occurrence of unidirectional block of the premature impulse, which, of course, is a prerequisite for the onset of circus movement. Furthermore, by use of a technique for synchronous multiple microelectrode recordings we obtained detailed information about the cellular responses during the initiation of the circus movement. 2 However, thus far no conclusive model of circus movement in the absence of an anatomical obstacle could be derived. This was due mainly to a lack of information about what happens in the center of a circulating impulse. In most studies on circus movement and reentry, the model introduced by Mines 3 in 1913 has been used. This model is based on observations in ring-shaped strips of cardiac tissue and implicitly supposes the presence of some kind of gross anatomical obstacle. However, in