Ashihara T, Yao T, Namba T, Ito M, Ikeda T, Kawase A, Toda S, Suzuki T, Inagaki M, Sugimachi M, Kinoshita M, Nakazawa K
First Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan.
J Cardiovasc Electrophysiol. 2001 Dec;12(12):1393-403. doi: 10.1046/j.1540-8167.2001.01393.x.
It is known that high-strength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as "electroporation." However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock.
Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the high-strength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation.
The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.
众所周知，高强度电击会破坏心肌细胞膜的脂质基质，并在膜上形成可逆的水性孔道。这个过程被称为“电穿孔”。然而，电穿孔是否有助于心室除颤机制仍不清楚。本计算机模拟研究的目的是探讨电穿孔在除颤电击成功中的可能作用。
使用改进的Luo-Rudy-1模型，我们模拟了具有均匀双域性质和不等各向异性比的二维心肌组织。通过S1-S2方法诱导螺旋波。接下来，通过两个线性电极从外部施加单相除颤电击。对于非电穿孔组织，正在进行的颤动终止成功；然而，即使使用高强度电击（24 V/cm），也会引发新的螺旋波。对于电穿孔组织，高强度电击（24 V/cm）足以消除正在进行的颤动，并且不会引发任何新的螺旋波。弱电击（16至20 V/cm）也能消除正在进行的颤动；然而，与高强度电击不同的是，会引发新的螺旋波。除颤成功取决于从物理阳极和虚拟阳极发生的电穿孔介导的阳极断相激发。电击后的一些兴奋波前使用兴奋性恢复的去极化区域作为通过点；因此，电穿孔介导的阳极断相激发对于阻断通过点是必要的，从而导致除颤成功。
电穿孔介导的阳极断相激发机制可能在电除颤中起重要作用。
