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V S Markhasin

Publications and source records attributed to V S Markhasin.

48 records · Page 3Linked to original sources
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[Modeling of mechanoelectric coupling in cardiomyocytes in norm and pathology].

We developed mathematical models of the electromechanical function of cardiomyocytes and the simplest mechanically heterogeneous myocardial systems, muscle duplexes. By means of these models we studied the contribution of mechanoelectric feedbacks to the contractile activity of the myocardium in norm and pathology. In particular, we simulated and clarified the effects of mechanical conditions on both the form and the duration of the action potential during contractions. From this standpoint different kinds of myocardium mechanical heterogeneity were analyzed. As we have established, the latter can play both a positive and a negative role, depending on the distribution of mechanical nonuniformity and the sequence of activation of heterogeneous myocardium system elements. By means of the same models, we studied the contribution of mechanical factors to the arrhythmogenicity in the case of the cardiomyocyte calcium overload caused by the attenuation of the sodium-potassium pump and outlined the ways for correcting the contractile function in these disturbances.

Action Potentials↗
PubMedDate not supplied

[Effect of heterogeneity of the myocardium on its mechanical function].

The influence of the mechanical heterogeneity on the myocardium contractility was evaluated. The heterogeneity was imitated by parallel connection of two papillar muscles with different mechanical properties. The rate of muscle shortening was controlled by a feed-back from tension of each of the muscles or both muscles simultaneously in the precision ergometer. The "force-velocity" and "length-force" relations were registered for each muscle independently, and in case of parallel connection of two muscles. It was shown that connection of two muscles in parallel influenced significantly the distribution of load in the muscles, maximal and mean velocity of their shortening. It is stated that the key phenomenon controlling the value and the heterogeneity influence sign is mechano-chemical uncoupling (inactivation).

Animals↗
PubMedDate not supplied

[The theory of regulation of the contraction force of the heart muscle].

A model of rhythmoinotropic phenomena in the heart muscle is elaborated. Kinetics of calcium flowing in intracellular pools of cardiomyocytes is described by differential equations. Dimensionless values (portions) serve as equation coefficients. They determine calcium kinetics in the pools and finally its amount is liberated into the myoplasm during stimulation. Proceeding from physiological considerations for portions there are given laws connecting portion values with intervals between stimuli. S-pool introduced into the model is principally new, it permits quantitative description of the effects of postextrasystolic potentiation and paired stimulation. Introduction of S-pool into the model changes the commonly accepted concept of calcium recirculation in the pools, and apparently, makes it possible for the first time to model all the results obtained on isolated myocardium of warm-blooded animals.

Action Potentials↗
PubMedDate not supplied

[Modeling the effect of rhythm on the strength of myocardial contraction].

A linear three-pool model of rhythm-inotropic phenomena in the cardiac muscle is proposed. Dynamics of accumulation and liberation of calcium from intracellular pools is described by differential equations. It has been shown by numerical experiments that rhythm-inotropic phenomena in the normal cardiac muscle and under cardiac insufficiency can be described qualitatively in terms of the concept on calcium recirculation in intracellular pools.

Action Potentials↗
PubMedDate not supplied

[The role of nonspecific troponin in kinetics of intracellular calcium in cardiomyocytes].

According to literature data nonspecific troponin TnC2 binds calcium in cardiac myocytes slowly and does not influence calcium transient. Therefore TnC2 often was not taken into consideration in models of the intracellular calcium kinetics. The mathematical model of the intracellular Ca(2+)-binding system we developed includes TnC2 as a ligand. Rate constants accepted for the complexation of Ca2+ by intracellular ligands give good agreement of the theoretical data with observed physiological ones. We compared the results of numerical experiments on this model with similar results obtained on the other model where TnC2 had been ignored. Some essential differences were revealed. In the model without TnC2 the fraction of calcium binding to specific troponin TnC1 always is smaller than the fraction of Ca2+ bound to the other ligands together. In our model TnC1 fraction (it regulates the mechanical response of muscle) is bigger that means more effective Ca(2+)-binding during activation of contractile proteins. The results above show that within the frame of our model the constants taken for Ca(2+)-binding ligands are more substantiate.

Calcium↗