抄録
To understand mechanisms of various functions of cardiac cells, the whole cell model was developed. The model is composed of ion channels, ion transporters, membrane receptors, coupling between the sarcolemmal Ca channel and the ryanodine receptor channels, sarcoplasmic reticulum with Ca, SERCA, calsequestrin, the contraction machinery, intracellular ion concentrations, mitochondria model, and gap junction channels. The function of these functional units are mostly described with experimenatal equations in literatures, otherwise model adjusted refering to experimental observations on macroscopic levels. The whole cell model, we call 'Kyoto Model', well reconstracts the pacemaker activity in the sinoatrial node cell, the ventricular action potential, the contraction, and homeostasis of the intracellular ion concentrations, energy metabolism and the cell volume regulation, classic regulation by the autonomic nervous transmitters. Responses to various experimental interventions are reversible. Model based new hypotheses were obtained for the pacemaker mechanisms, cell volume regulation via ion fluxes through sarcolemma, and the Ca mediated upregulation of the mitochondrial ATP production on increasing the work load. The model still needs to be revised and implemented with new mechanisms, thereby the integrations of the experimental knowledge will be most efficiently and systematicall achieved through developing the whole cell model. All these model constructions were conducted on simBio, which is newly developed Java package by us for constructing cell models on a large scale (http://www.sim-bio.org/). [J Physiol Sci. 2006;56 Suppl:S3]
