Department of Physiology, University of Bern, Bern, Switzerland.
Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Institute of Microengineering, Institute of Bioengineering, Centre for Neuroprosthetics, École Polytechnique Fédérale de Lausanne (EPFL), Geneva, Switzerland.
Acta Physiol (Oxf). 2018 May;223(1):e13026. doi: 10.1111/apha.13026. Epub 2018 Jan 15.
Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perpendicular to impulse propagation.
Cardiomyocyte strands were cultured on stretchable custom microelectrode arrays, and θ was determined during steady-state pacing. Uniaxial strain (5%) with principal axis parallel (orthodromic) or perpendicular (paradromic) to propagation was applied for 1 minute and controlled by imaging a grid of markers. The results were analysed in terms of cable theory.
Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (P < .001) than paradromic strain (2.2 ± 0.5% vs 1.0 ± 0.2% in n = 8 mouse cardiomyocyte cultures, 2.3 ± 0.4% vs 0.9 ± 0.5% in n = 4 rat cardiomyocyte cultures, respectively). The larger effect of orthodromic strain can be explained by the increase in axial myoplasmic resistance, which is not altered by paradromic strain. Thus, changes in tissue resistance substantially contributed to the changes of θ during strain, in addition to other influences (eg stretch-activated channels). Besides these immediate effects, the application of strain also consistently initiated a slow progressive decrease in θ and a slow recovery of θ upon release.
Changes in cardiac conduction velocity caused by acute stretch do not only depend on the magnitude of strain but also on its orientation relative to impulse propagation. This dependence is due to different effects on tissue resistance.
心肌组织变形可改变组织电阻、膜电容和离子电流，从而导致致心律失常性缓慢传导。我们的目的是研究当主应变轴与冲动传播平行或垂直时，单向应变是否会导致传导速度（θ）发生不同的变化。
心肌细胞条带在可拉伸的定制微电极阵列上培养，并在稳态起搏期间确定 θ。施加 5%的单向应变（平行于传播方向为顺行性，垂直于传播方向为逆行性），主应变轴 1 分钟，并通过成像网格标记物进行控制。结果根据电缆理论进行分析。
两种类型的应变在施加和释放时都会立即引起 θ 的变化。在材料坐标中，顺行应变比逆行应变显著降低θ（P<.001）（在 n=8 个鼠心肌细胞培养物中分别为 2.2±0.5%和 1.0±0.2%，在 n=4 个大鼠心肌细胞培养物中分别为 2.3±0.4%和 0.9±0.5%）。顺行应变的更大影响可以用轴向细胞质电阻的增加来解释，而逆行应变不会改变轴向细胞质电阻。因此，在应变过程中，除了其他影响因素（例如拉伸激活通道）外，组织电阻的变化也会显著影响 θ 的变化。除了这些即时效应外，应变的施加还会持续引发 θ 的缓慢渐进性降低和释放后的缓慢恢复。
急性拉伸引起的心脏传导速度变化不仅取决于应变的大小，还取决于其相对于冲动传播的方向。这种依赖性归因于对组织电阻的不同影响。
