Rosenshtraukh L V, Zaitsev A V, Fast V G, Pertsov A M, Krinsky V I
Institute of Experimental Cardiology, All-Union Cardiology Research Center, Moscow, USSR.
J Mol Cell Cardiol. 1991 Feb;23 Suppl 1:3-9. doi: 10.1016/0022-2828(91)90018-h.
It is known that parasympathetic influence favors induction of re-entrant atrial tachycardias (ATs). This effect is usually interpreted as a result of inhomogeneous shortening of atrial refractoriness leading to increased probability of circus movement following a premature impulse. However, early microelectrode studies showed that in spontaneously beating isolated frog atria, intensive vagal stimulation (VS) induced paroxysms of rapid AT in the absence of myocardial extrastimulation. This AT was found to correlate with inexcitability of some of the impaled fibers of the atria. It was supposed that temporary, vagally induced, inexcitable areas of the atria could lead to re-entry, serving as a site of unidirectional conduction. This hypothesis was recently evaluated by direct multielectrode mapping of excitation sequence during vagally induced AT in frog atria. Recording from 32 sites with a spatial resolution of 1-2 mm clearly showed that the AT was due to re-entry. The ATs were always preceded by vagally induced depression of conduction, with some areas of the atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner. The re-entrant AT was initiated when a sinus impulse arrived during a certain phase of the recovery. Unlike the well-known mechanism of re-entry, which is based on inhomogeneous refractoriness and extrabeat(s), the re-entrant AT in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.
已知副交感神经的影响有利于折返性房性心动过速（ATs）的诱发。这种效应通常被解释为心房不应期不均匀缩短的结果，导致早搏后发生折返运动的可能性增加。然而，早期的微电极研究表明，在自发搏动的离体蛙心房中，强烈的迷走神经刺激（VS）在没有心肌额外刺激的情况下诱发了快速AT的阵发性发作。发现这种AT与心房中一些被刺穿纤维的兴奋性丧失有关。据推测，迷走神经诱导的心房暂时兴奋性丧失区域可能导致折返，作为单向传导的部位。最近，通过对蛙心房迷走神经诱导的AT期间兴奋序列的直接多电极标测，对这一假说进行了评估。以1-2毫米的空间分辨率从32个部位进行记录，清楚地表明AT是由折返引起的。AT发作之前总是先出现迷走神经诱导的传导抑制，心房的一些区域完全阻滞。随着迷走神经影响的减弱，阻滞区域以不均匀的方式恢复。当窦性冲动在恢复的某个阶段到达时，折返性AT就会开始。与基于不应期不均匀和早搏的众所周知的折返机制不同，我们模型中的折返性AT依赖于迷走神经诱导的传导阻滞，并且可以由单个窦性冲动引发。
