Rabbit-specific computational modelling of ventricular cell electrophysiology: Using populations of models to explore variability in the response to ischemia.
Rabbit-specific computational modelling of ventricular cell electrophysiology: Using populations of models to explore variability in the response to ischemia.
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DOI：
10.1016/j.pbiomolbio.2016.06.003
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发表时间：
2016-07
影响因子：
3.8
通讯作者：
Quinn TA
中科院分区：
文献类型：
--
作者：
Gemmell P;Burrage K;Rodríguez B;Quinn TA
计算模型与实验研究相结合，是研究复杂心脏电生理行为的有效方法。由于这一物种的心脏电生理学与人类相似，使用兔特有的模型尤其普遍。在这篇文章中，我们首先简要回顾了特定于兔的计算模型的心室细胞电生理学，多细胞模拟包括细胞异质性和急性缺血。在这篇简短的综述之后，对两组实验校准的兔特定的心室肌细胞动作电位模型对急性缺血的电生理反应的变异性进行了原始的计算调查。我们对模型人群对不同程度的缺血和个体缺血参数的反应进行了系统的探索，以研究它们对动作电位时程和不应性的单独和联合影响。这揭示了模型群体变异性和缺血因素之间复杂的相互作用，它们结合在一起增强了缺血期间的变异性。这代表着朝着更好地理解生理变异性在急性缺血期间电生理改变中可能发挥的作用迈出了重要的一步。
Computational modelling, combined with experimental investigations, is a powerful method for investigating complex cardiac electrophysiological behaviour. The use of rabbit-specific models, due to the similarities of cardiac electrophysiology in this species with human, is especially prevalent. In this paper, we first briefly review rabbit-specific computational modelling of ventricular cell electrophysiology, multi-cellular simulations including cellular heterogeneity, and acute ischemia. This mini-review is followed by an original computational investigation of variability in the electrophysiological response of two experimentally-calibrated populations of rabbit-specific ventricular myocyte action potential models to acute ischemia. We performed a systematic exploration of the response of the model populations to varying degrees of ischemia and individual ischemic parameters, to investigate their individual and combined effects on action potential duration and refractoriness. This revealed complex interactions between model population variability and ischemic factors, which combined to enhance variability during ischemia. This represents an important step towards an improved understanding of the role that physiological variability may play in electrophysiological alterations during acute ischemia.