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Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Buccarello A., Azzarito M., Michoud F., Lacour S. P., Kucera J. P.,
Project Bioelectrical-biomechanical interactions in cardiac tissue and ephaptic conduction: two challenging aspects of cardiac electrophysiology
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Original article (peer-reviewed)

Journal Acta Physiologica
Volume (Issue) 223(1)
Page(s) e13026 - e13026
Title of proceedings Acta Physiologica
DOI 10.1111/apha.13026

Open Access

URL https://boris.unibe.ch/108793/
Type of Open Access Repository (Green Open Access)

Abstract

Aim: 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. Methods: 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 min and controlled by imaging a grid of markers. The results were analysed in terms of cable theory. Results: Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (p<0.001) 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 of 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 (e.g., stretch-activated channels). Besides these immediate effects, the application of strain also consistently initiated a slow progressive decrease of θ and a slow recovery of θ upon release. Conclusion: 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.
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