首页> 外文会议>International Workshop on Functional Imaging and Modeling of the Heart(FIMH 2007); 20070607-09; Salt Lake City,UT(US) >Mathematical Modeling of Electromechanical Function Disturbances and Recovery in Calcium-Overloaded Cardiomyocytes
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Mathematical Modeling of Electromechanical Function Disturbances and Recovery in Calcium-Overloaded Cardiomyocytes

机译:钙超负荷心肌细胞中机电功能扰动和恢复的数学模型

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摘要

Rhythm disturbances and mechanical function suppression proper to the acute heart failure in the case of cardiomyocyte calcium overload are simulated in a mathematical model of cardiomyocyte electromechanical activity. Particular attention is paid to the overload caused by diminished activity of the Na~+-K~+ pump. It is shown in the framework of the model that myocardium mechanics may promote arrhythmias in these conditions. In particular, cooperative influence of the attached crossbridges on the calciumtroponin kinetics is shown to contribute to the initiation of spontaneous action potentials. Numerical experiments showed that the recovery of the normal Na~+-K~+ pump activity during the heart failure attack did not always led to the normal electromechanical function recovery in the failed cardiomyocyte. Alternative approaches were suggested in the model and compared to each other for recovery of the myocardium electrical and mechanical performance in the simulated case of the acute heart failure.
机译:在心肌细胞机电活动的数学模型中,模拟了心肌细胞钙超载时适用于急性心力衰竭的节律紊乱和机械功能抑制。特别要注意由Na〜+ -K〜+泵的活动减少引起的过载。在模型的框架中显示,心肌力学可在这些情况下促进心律不齐。特别地,显示出所连接的跨桥对钙钙蛋白动力学的协同影响有助于自发动作电位的启动。数值实验表明,在心力衰竭发作期间恢复正常的Na〜+ -K〜+泵活动并不总是导致失败的心肌细胞恢复正常的机电功能。在模型中提出了替代方法,并在模拟的急性心力衰竭病例中将它们相互比较以恢复心肌的电和机械性能。

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