In order to increase the knowledge about heart and its physiology, a great number of experimental activities have being conducted. Part of such activities analyses single myocardial cells; usually, these processes present a lot of complications mainly concerning myocytes isolation, low reproducibility and high number of system related variables. Basing on these considerations the present work refers to the development of a numerical model of myocyte that permits to simulate its physiological contraction as well as pathological behaviours. The analysis of the single myocyte (the basic unit of cardiac tissue) is necessary to investigate heart as a single complex system in order to develop a numerical heart model able to simulate either the physiological and the pathological behaviour and thus overcome the experimental trials. The model enables the evaluation of contractility under three inotropic substances effect: angiotensin-II, endothelin-I and isoproterenol. It has been developed in three phases: an initial analysis of the behaviour of the sarcomere has been executed and a sarcomere model has been developed, such model permits to simulate both physiological activity of sarcomere and to analyze the inotropic effect of the three substances on it; finally a model of myocyte has been elaborated using both experimental data obtained from several trials previously defined and literature data; at the end the model has been validated both with literature results and with data obtained from subsequent experimental trials.
[1]
A. Hill.
The heat of shortening and the dynamic constants of muscle
,
1938
.
[2]
G. Piazzesi,et al.
The stiffness of skeletal muscle in isometric contraction and rigor: the fraction of myosin heads bound to actin.
,
1998,
Biophysical journal.
[3]
R Pietrabissa,et al.
A model of multicomponent cardiac fibre.
,
1987,
Journal of biomechanics.
[4]
J. Willerson,et al.
Contraction and resting stiffness of isolated cardiac muscle: effects of inotropic agents.
,
1977,
American Journal of Physiology.
[5]
W. Lew,et al.
Lipopolysaccharide depresses cardiac contractility and beta-adrenergic contractile response by decreasing myofilament response to Ca2+ in cardiac myocytes.
,
1997,
Circulation research.
[6]
R. Pietrabissa,et al.
Mechanical characterization of a model of a multicomponent cardiac fibre.
,
1991,
Journal of biomedical engineering.
[7]
C. Poggesi,et al.
Active and passive forces of isolated myofibrils from cardiac and fast skeletal muscle of the frog.
,
1997,
The Journal of physiology.
[8]
P. Burton,et al.
Effect of protein kinase A on calcium sensitivity of force and its sarcomere length dependence in human cardiomyocytes.
,
2000,
Cardiovascular research.