• Proceedings of the Korean Society of Precision Engineering Conference
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• 2004.10a
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• pp.1176-1179
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• 2004

A new cell-cross bridge mechanics model is proposed to analyze the mechanics of heart muscle. Electrophysiology of a cardiac cell is numerically approximated using the previous model of human ventricular myocyte. Ion transports across cell membrane initiated by action potential induce excitation-contraction mechanism in the cell via cross bridge dynamics. Negroni and Lascano model (NL model) is employed to compute the tension of cross bridge closely related to ion dynamics in cytoplasm.

• Proceedings of the KSME Conference
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• 2007.05b
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• pp.2947-2950
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• 2007

A 3D human ventricular model is proposed to simulate an integrative analysis of heart physiology and blood hemodynamics. This consists of the models of electrophysiology of human cells, electric wave propagation of tissue, heart solid mechanics, and 3D blood hemodynamics. The 3D geometry of human heart is discretized to a finite element mesh for the simulation of electric wave propagation and mechanics of heart. In cellular level, excitations by action potential are simulated using the existing human model. Then the contraction mechanics of a whole cell is incorporated to the excitation model. The excitation propagation to ventricular cells are transiently computed in the 3D cardiac tissue using a mono-domain method of electric wave propagation in cardiac tissue. Blood hemodynamics in heart is also considered and incorporated with muscle contraction. We use a PISO type finite element method to simulate the blood hemodynmaics in the human ventricular model.

• Journal of Institute of Control, Robotics and Systems
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• v.10 no.12
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• pp.1164-1171
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• 2004

A new multi-scale simulation model is proposed to analyze heart mechanics. Electrophysiology of a cardiac cell is numerically approximated using the previous model of human ventricular myocyte. The ion transports across cell membrane initiated by action potential induce an excitation-contraction mechanism in the cell via cross bridge dynamics. Negroni and Lascano model (NL model) is employed to calculate the tension of cross bridge which is closely related to the ion dynamics in cytoplasm. To convert the tension on cell level into contraction force of cardiac muscle, we introduce a simple geometric model of ventricle with a thin-walled hemispheric shape. It is assumed that cardiac tissue is composed of a set of cardiac myocytes and its orientation on the hemispheric surface of ventricle remains constant everywhere in the domain. Application of Laplace law to the ventricle model enables us to determine the ventricular pressure that induces blood circulation in a body. A lumped parameter model with 7 compartments is utilized to describe the systemic circulation interacting with the cardiac cell mechanism via NL model and Laplace law. Numerical simulation shows that the ion transports in cell level eventually generate blood hemodynamics on system level via cross bridge dynamics and Laplace law. Computational results using the present multi-scale model are well compared with the existing ones. Especially it is shown that the typical characteristics of heart mechanics, such as pressure volume relation, stroke volume and ejection fraction, can be generated by the present multi-scale cardiovascular model, covering from cardiac cells to circulation system.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.279-284
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• 1995

The aim of the present study was to know whether exogenously administered nitric oxide (NO) may differently modulate muscle mechanics between heart and aorta. We used PIANO method to generate NO. In isolated rat atrial tissues, neither heart rate nor contractility was affected by PIANO $(STZ,\;30{\sim}100\;{\mu}M)$. Only high concentration $(100\;{\mu}M)$ of 8-bromo cyclic GMP slightly depressed cardiac contractility. However, the same concentrations of 8-Br cGMP and PIANO significantly relaxed the rat thoracic aorta contracted with phenylephrine $(0.1\;{\mu}M)$. In isolated rabbit cardiac atrial myocytes, the amplitude of calcium currents were decreased in the whole voltage range by the presence of streptozotocin, which was further potentiated by UV light. Calcium currents were also decreased in those preparations treated with bradykinin, nitroprusside and 8-Br cGMP. These findings suggest that exogenous NO may modulate calcium current in cardiac myocyte. However, it remains why this does not affect myocardial contractility and heart rate. We concluded that NO may differently regulate calcium signal between aorta and heart muscle.