The geometry of excitation wave front may play an important role on the propagation block and spiral wave formation. The wave front which is bent over the critical value due to interaction with the obstacles may partially cease to propagate and appearing wave breaks evolve into rotating waves or reentry. This scenario may explain how reentry spontaneously originates in a heart. We studied highly curved excitation wave fronts in the cardiac tissue culture and found that in the conditions of normal, non-inhibited excitability the curvature effects do not play essential role in the propagation. Neither narrow isthmuses nor sharp corners of the obstacles, being classical objects for production of extremely curved wave front, affect non-inhibited wave propagation. The curvature-related phenomena of the propagation block and wave detachment from the obstacle boundary were observed only after partial suppression of the sodium channels with Lidocaine. Computer simulations confirmed the experimental observations. The explanation of the observed phenomena refers to the fact that the heart tissue is made of finite size cells so that curvature radii smaller than the cardiomyocyte size loses sense, and in non-inhibited tissue the single cell is capable to transmit excitation to its neighbors.

中文翻译：

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培养的心脏组织中曲率依赖性兴奋性传播。

激发波阵面的几何形状可能对传播块和螺旋波形成起重要作用。由于与障碍物的相互作用而弯曲超过临界值的波阵面可能会部分停止传播，并且出现的波折会演变成旋转波或折返。这种情况可能解释了折返是如何自发地起源于心脏的。我们研究了心脏组织培养物中高度弯曲的激发波波前，发现在正常的，非抑制性的兴奋性条件下，曲率效应在传播过程中不起关键作用。狭窄的峡部和障碍物的尖角都不是产生极弯曲波前的经典物体，不会影响非抑制波的传播。仅在利多卡因钠通道被部分抑制后，才观察到传播块的曲率相关现象和波从障碍物边界脱离。计算机模拟证实了实验观察。对观察到的现象的解释是指这样的事实，即心脏组织是由有限大小的细胞组成的，因此小于心肌细胞大小的曲率半径就失去了意义，并且在非抑制性组织中，单个细胞能够将兴奋性传递至周围的细胞。