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Front Physiol. 2017 Mar 30;8:195. doi: 10.3389/fphys.2017.00195. eCollection 2017.

Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.

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School of Computer Science and Technology, Harbin Institute of TechnologyHarbin, China.
State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of TechnologyHarbin, China.
Biological Physics Group, School of Physics and Astronomy, University of ManchesterManchester, UK.
Space Institute of Southern ChinaShenzhen, China.


Acidosis has complex electrophysiological effects, which are associated with a high recurrence of ventricular arrhythmias. Through multi-scale cardiac computer modeling, this study investigated the mechanisms underlying the emergence of post-acidosis arrhythmia at the tissue level. In simulations, ten Tusscher-Panfilov ventricular model was modified to incorporate various data on acidosis-induced alterations of cellular electrophysiology and intercellular electrical coupling. The single cell models were incorporated into multicellular one-dimensional (1D) fiber and 2D sheet tissue models. Electrophysiological effects were quantified as changes of action potential profile, sink-source interactions of fiber tissue, and the vulnerability of tissue to the genesis of unidirectional conduction that led to initiation of re-entry. It was shown that acidosis-induced sarcoplasmic reticulum (SR) calcium load contributed to delayed afterdepolarizations (DADs) in single cells. These DADs may be synchronized to overcome the source-sink mismatch arising from intercellular electrotonic coupling, and produce a premature ventricular complex (PVC) at the tissue level. The PVC conduction can be unidirectionally blocked in the transmural ventricular wall with altered electrical heterogeneity, resulting in the genesis of re-entry. In conclusion, altered source-sink interactions and electrical heterogeneity due to acidosis-induced cellular electrophysiological alterations may increase susceptibility to post-acidosis ventricular arrhythmias.


delayed afterdepolarization; post acidosis arrhythmias; premature ventricular complexes; sink-source mismatch; transmural dispersion of repolarization; ventricular tachycardia

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