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
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.