MATHEMATICAL-MODELING OF THE CONTRIBUTION OF MECHANICAL INHOMOGENEITYIN THE MYOCARDIUM TO CONTRACTILE FUNCTION

Citation
Vs. Markhasin et al., MATHEMATICAL-MODELING OF THE CONTRIBUTION OF MECHANICAL INHOMOGENEITYIN THE MYOCARDIUM TO CONTRACTILE FUNCTION, General physiology and biophysics, 16(2), 1997, pp. 101-137
Citations number
14
Categorie Soggetti
Physiology,Biophysics
ISSN journal
02315882
Volume
16
Issue
2
Year of publication
1997
Pages
101 - 137
Database
ISI
SICI code
0231-5882(1997)16:2<101:MOTCOM>2.0.ZU;2-H
Abstract
Earlier we developed a mathematical model of the cardiac muscle that a llowed for inactivation through the effects of cooperativity of contra ctile proteins. In the present work we used the model to analyze the m echanical function of an inhomogeneous myocardium. To simulate the lat ter we chose, as the simplest system, a duplex in which muscles with d ifferent mechanical properties were connected in series and in paralle l. Numerical experiments showed that the basic effect due to the inhom ogeneity consists in the non-additivity of the mechanical characterist ics of the muscle, e. g., of the relationship between end-systolic len gth and end-systolic force (L-es - P-es). As a rule, non-additivity co nsists in a negative inotropic effect. The analysis showed that the ca use of non-additivity is redistribution of loads between muscles (in a parallel duplex), redistribution of lengths (in a serial duplex), cha nges in the rate of contraction of each muscle compared to contraction that when working separately, shifts in time to L-es. Also, the model predicts that additional inactivation of contractile proteins in a mu scle within a duplex against isolation is the substantial mechanism of enhanced non-additivity. Among the factors of inhomogeneity studied t he basic determinants are difference in amplitudes between isometric t ensions developed by each muscle in isolation and the asynchronism in the development of these tensions.