Mathematical model of the electromechanical heart contractile system--regulatory subsystem physiological considerations.

Mathematical model of the electromechanical heart contractile system--regulatory subsystem physiological considerations.
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机电心脏收缩系统的数学模型——调节子系统的生理考虑。

DOI:
10.33549/physiolres.930105
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发表时间:
2001
影响因子:
2.1
通讯作者:
V. Novák
V. Novák
中科院分区:
医学4区
文献类型:
--
作者:
M. Mlček;J. Neumann;O. Kittnar;V. Novák

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提出了心肌细胞兴奋-收缩耦合的生化模型,并讨论了模拟生理和病理过程的有效性。调节和肌动球蛋白子系统的模型,即使它是相当简单的,在其调节亚基,给出的结果与实验数据一致。具体而言,细胞内游离钙水平([Ca 2 +]i)的肌内质网Ca 2 +-ATP酶(SERCA 2)的各种状态下计算,并与实验结果进行比较。计算结果很好地再现了心力衰竭中常见的静息[Ca ~(2+)]i水平的升高和[Ca ~(2+)]i下降的衰减。因此,计算模拟可以帮助确定研究系统中的核心关系,通过比较使用不同复杂性的类似模型获得的结果。
The biochemical model of excitation-contraction coupling in cardiomyocyte is presented and the validity of simulations of both physiological and pathological processes is discussed. The model of regulatory and actomyosin subsystems, even if it is rather simple in its regulatory subunit, gives results well consistent with experimental data. Specifically, intracellular free calcium levels ([Ca2+]i) were computed under various states of sarcoendoplasmic reticular Ca2+-ATPase (SERCA2) and compared to experimental findings. Computed results reproduced well both the increase in resting [Ca2+]i level and the attenuation of [Ca2+]i decline commonly observed in heart failure. Thus the computational simulations could help to identify core relations in studied systems by comparing results obtained using similar models of various complexities.
DOI: 10.1016/s0022-2828(84)80702-6
发表时间: 1984
影响因子: 5
作者:
Eisner,DA;Orchard,CH;Allen,DG
通讯作者: Allen,DG
DOI: 10.1152/ajpheart.1999.276.5.h1734
发表时间: 1999-05-01
影响因子: 4.8
作者:
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通讯作者: Hunter, WC
DOI: 10.1016/s0006-3495(81)84868-0
发表时间: 1981-01-01
影响因子: 3.4
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通讯作者: POTTER, JD