Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.
Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.
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组织水平酸中毒后心律失常出现的机制：理论研究
DOI：
10.3389/fphys.2017.00195
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发表时间：
2017
影响因子：
4
通讯作者：
Zhang H
中科院分区：
文献类型：
--
作者：
Bai J;Yin R;Wang K;Zhang H
酸中毒具有复杂的电生理效应，与室性心律失常的高复发率相关。通过多尺度心脏计算机模拟，本研究在组织水平上研究了酸中毒后心律失常出现的机制。在模拟中，十Tusscher-Panfilov心室模型进行了修改，以纳入各种数据酸中毒引起的细胞电生理学和细胞间电耦合的变化。将单细胞模型并入多细胞一维（1D）纤维和2D片状组织模型中。电生理学效应被量化为动作电位曲线的变化、纤维组织的汇-源相互作用以及组织对导致折返起始的单向传导的发生的脆弱性。结果表明，酸中毒诱导的肌浆网（SR）钙负荷有助于延迟后除极（DADs）的单细胞。这些DAD可以被同步以克服由细胞间电紧张性耦合引起的源-汇失配，并在组织水平产生室性早搏复合波（PVC）。PVC传导可以在透壁心室壁中单向阻断，改变电异质性，导致折返的发生。总之，酸中毒诱导的细胞电生理学改变导致的源-汇相互作用和电异质性改变可能会增加酸中毒后室性心律失常的易感性。
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.