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Shimayoshi T.,ASTEM Research Institute of Kyoto | Hasegawa Y.,Kyoto University | Mishima M.,Kyoto University | Matsuda T.,Kyoto University
IET Systems Biology | Year: 2013

Energetic efficiency is an important indicator of cardiac function in acute myocardial infarction. However, the relationship between cardiac energetic efficiency and infarct size is not perfectly elucidated. In this study, the relationship is analysed by means of simulation using a theoretical model of the guinea pig left ventricle. In simulation with varied ratios of infarct area, pressure-volume area (PVA), which is an index of total mechanical energy by ventricular contraction, and myocardial oxygen consumption (MVO2) are calculated for each infarct ratio. Then, change of PVA when MVO2 alters (PVA/MVO2) as a well-known index of energy conversion efficiency is evaluated. In addition, PVA/VO2, which represents a ratio of PVA change to alteration of mean oxygen consumption of myocytes except for infarct myocytes, is introduced as an index for real energetic efficiency. In simulation results, PVA/MVO2 increases but PVA/VO2 decreases as infarct area expands, because with expansion of infarct area PVA decreases but VO2 remains almost unchanged because of larger shortening of myocytes. This implies that the enlargement of shortening of noninfarcted myocyte to compensate for depression of cardiac output is a potential cause of myocardial remodelling. © The Institution of engineering and technology 2013. Source

Punzalan F.R.,Ritsumeikan University | Yamashita Y.,Ritsumeikan University | Soejima N.,Ritsumeikan University | Kawabata M.,Ritsumeikan University | And 4 more authors.
Source Code for Biology and Medicine | Year: 2012

Models written in description languages such as CellML are becoming a popular solution to the handling of complex cellular physiological models in biological function simulations. However, in order to fully simulate a model, boundary conditions and ordinary differential equation (ODE) solving schemes have to be combined with it. Though boundary conditions can be described in CellML, it is difficult to explicitly specify ODE solving schemes using existing tools. In this study, we define an ODE solving scheme description language-based on XML and propose a code generation system for biological function simulations. In the proposed system, biological simulation programs using various ODE solving schemes can be easily generated. We designed a two-stage approach where the system generates the equation set associating the physiological model variable values at a certain time t with values at t + Δt in the first stage. The second stage generates the simulation code for the model. This approach enables the flexible construction of code generation modules that can support complex sets of formulas. We evaluate the relationship between models and their calculation accuracies by simulating complex biological models using various ODE solving schemes. Using the FHN model simulation, results showed good qualitative and quantitative correspondence with the theoretical predictions. Results for the Luo-Rudy 1991 model showed that only first order precision was achieved. In addition, running the generated code in parallel on a GPU made it possible to speed up the calculation time by a factor of 50. The CellML Compiler source code is available for download at http://sourceforge.net/projects/cellmlcompiler. © 2012 Punzalan et al.; licensee BioMed Central Ltd. Source

Shimayoshi T.,ASTEM Research Institute of Kyoto | Kubota Y.,Kyoto University | Amano A.,Ritsumeikan University | Matsuda T.,Kyoto University
Transactions of Japanese Society for Medical and Biological Engineering | Year: 2013

Detailed analysis of oxygen consumption within the myocardial microcirculation is of importance to understand conditions under ischemic heart disease. However, there are currently difficulties in microscopically precise measurements of local oxygen consumptions in myocardial tissue. In this paper, a simulation model of myocardial microcirculation is proposed for analysis of local distribution of oxygen consumption. The proposed model is composed by integrating a theoretical spatially-distributed model of myocardial tissue and a detailed lumped-parameter model of normal cardiac myocyte. The proposed model was validated for an animal research in reproduction of a linear correlation between myocardial oxygen consumption and myocardial contractility. A simulation result of the model shows that local oxygen consumptions under low myocardial blood flow are spatially partitioned into an arteriolar-side normal area and a venular-side low area. Myocytes in the venular-side area lose normal activity under extremely low oxygen concentration. This result indicates the possibility that cardiac tissue is locally damaged under extreme hypoxia in the venular-side area even in case of a slight reduction of mean oxygen consumption of the myocadial tissue caused by decreased myocardial blood flow. Source

Cha C.Y.,Ritsumeikan University | Santos E.,Ritsumeikan University | Amano A.,Ritsumeikan University | Shimayoshi T.,ASTEM Research Institute of Kyoto | Noma A.,Ritsumeikan University
Journal of General Physiology | Year: 2011

In our companion paper, the physiological functions of pancreatic β cells were analyzed with a new β-cell model by time-based integration of a set of differential equations that describe individual reaction steps or functional components based on experimental studies. In this study, we calculate steady-state solutions of these differential equations to obtain the limit cycles (LCs) as well as the equilibrium points (EPs) to make all of the time derivatives equal to zero. The sequential transitions from quiescence to burst-interburst oscillations and then to continuous firing with an increasing glucose concentration were defined objectively by the EPs or LCs for the whole set of equations. We also demonstrated that membrane excitability changed between the extremes of a single action potential mode and a stable firing mode during one cycle of bursting rhythm. Membrane excitability was determined by the EPs or LCs of the membrane subsystem, with the slow variables fixed at each time point. Details of the mode changes were expressed as functions of slowly changing variables, such as intracellular [ATP], [Ca2+], and [Na+]. In conclusion, using our model, we could suggest quantitatively the mutual interactions among multiple membrane and cytosolic factors occurring in pancreatic β cells. © 2011 Cha et al. Source

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