Computer model of membrane current and intracellular Ca2+ flux in the isolated guinea pig ventricular myocyte.
Computer model of membrane current and intracellular Ca2+ flux in the isolated guinea pig ventricular myocyte.
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DOI：
10.1152/ajpheart.1993.265.6.h2117
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发表时间：
1993-12
期刊：
影响因子：
--
通讯作者：
C. Nordin
中科院分区：
文献类型：
--
作者：
C. Nordin
本文给出了一个数学模型的方程和响应，该模型模拟了离体豚鼠心肌细胞的跨膜电流和胞内Ca 2+（[Ca 2 +]）、Na+（[Na+]）和K+（[K+]）浓度。该模型的结构与DiFrancesco和Noble的公式密切相关（9）。定量值是基于大量的实验限制，从文献中分离的肌细胞以及我们自己的实验研究，描述了各种条件下的单个通道和整个细胞的综合反应的属性。该模型被构建为一个稳态系统。该模型的平衡对应于未受刺激的肌细胞的静息电位和细胞内离子浓度。该模型产生偏离平衡对应的细胞行为刺激后的动作电位在不同的利率，钠-钾-腺苷三磷酸酶（ATP酶）的封锁，减少细胞外[K+]，并注入恒定的去极化电流。该模型的模拟结果表明，在不同的刺激率下，肌浆[Ca 2 +]的变化，恢复和期外收缩后增强的产生，以及细胞内[Ca 2 +]振荡的发展，仅仅是由于Ca（2+）-ATP酶将Ca 2+摄取到肌浆网，Ca（2+）诱导的Ca 2+释放到肌浆，摄取和释放区域之间的通量，以及肌浆网和肌浆之间的渗漏。该模型还表明，各种各样的基本电生理反应的离体豚鼠心肌细胞可以模拟与定量精度由一组方程的基础上实验测得的跨膜电流和细胞内[Ca 2 +]和[Na+]。
This paper presents the equations and responses of a mathematical model that simulates the transmembrane current and intracellular concentrations of Ca2+ ([Ca2+]), Na+ ([Na+]), and K+ ([K+]) of an isolated guinea pig myocyte. The structure of the model is closely related to the formulation of DiFrancesco and Noble (9). Quantitative values are based on a large number of experimental constraints, taken from the literature on isolated myocytes as well as our own experimental studies, that describe the properties of individual channels and integrated responses of whole cells under a variety of conditions. The model was constructed as a homeostatic system. The equilibrium of the model corresponds to the resting potential and intracellular ionic concentrations of unstimulated myocytes. The model generates deviations from equilibrium corresponding to the behavior of cells after stimulation of action potentials at different rates, blockade of Na-K-adenosinetriphosphatase (ATPase), reduction in extracellular [K+], and injection of constant depolarizing current. Simulations from the model suggest that changes in myoplasmic [Ca2+] at different stimulation rates, the generation of restitution and postextrasystolic potentiation, and the development of intracellular [Ca2+] oscillations arise simply from different interactions between uptake of Ca2+ into the sarcoplasmic reticulum via the Ca(2+)-ATPase, Ca(2+)-induced Ca2+ release of Ca2+ into the myoplasm, flux between regions of uptake and release, and leakage between sarcoplasmic reticulum and myoplasm. The model also demonstrates that a wide variety of basic electrophysiological responses of the isolated guinea pig myocyte can be simulated with quantitative precision by a single set of equations based on experimentally measured transmembrane current and intracellular [Ca2+] and [Na+].