Reentrant Action Potentials in Normal Myocardium

尽管健康的心肌在亚毫米和亚毫秒尺度上结构和功能明显不连续，但它的行为更像是一个连续的、均匀的可兴奋介质。在此类比和相应的数值模型的基础上，已经预测到心肌在一定的相位和大小的刺激下是脆弱的，这种刺激导致二维成对涡旋和三维涡丝形式的折返，而与明显使病变组织更脆弱的不连续性和异质性无关。这一结果和相关结果现已通过电刺激和高分辨率心肌标测得到证实。下一个支持间隔的目的是：(1)像以前一样，通过数值计算和与实验生理学家合作，探索三维涡度的含义；(2)通过现有最好的心室心肌膜电生理模型的解释透镜来检验这些现象；(3)利用这些电生理膜模型，了解折返性心动过速发展为纤颤的可兴奋介质的非线性动力学；(4)从理论角度考察除颤的可能机制，从而巩固。通过对感兴趣的特定可激发介质的特定离子机制进行计算建模，应该可以第一次定量地详细了解这些机制。这将使人们能够通过改变电场来理解和控制膜的性质。

Healthy ventricular myocardium behaves much like a continuous uniform excitable medium, despite its evident discontinuities of structure and function on sub-mm and sub-msec scales. On the basis of this analogy and the corresponding numerical models it has been predicted that myocardium should be vulnerable to a stimulus of certain phase and size which induces reentry in the form of paired vortices in 2 dimensions and vortex filaments in 3 dimensions, independent of the discontinuities and heterogeneity that apparently make diseased tissue more vulnerable. This and related consequences have now been confirmed by electrical stimulation and high-resolution myocardial mapping. The purposes for the next support interval are (1) to explore the implications for 3- dimensional vorticity, both numerically and in collaboration with experimental physiologists, as before; (2) to examine these phenomena through the interpretive lens of the best available electrophysiological model of ventricular myocardial membrane; (3) to understand the development of reentrant tachycardias into fibrillation in terms of the nonlinear dynamics of excitable media, using those electrophysiological membrane models; and (4) to examine possible mechanisms of defibrillation from the theoretical perspective thus consolidated. By computational modelling of specific ionic mechanisms of the particular excitable medium of interest, it should be possible to understand these mechanisms in quantitative detail for the first time. This will allow an understanding and control of membrane properties via altered electric fields.