Analytical model for predicting mechanotransduction effects in engineered cardiac tissue.
Mechanochemical and mechanoelectrical signaling is imperative for cardiac organogenesis and underlies pathophysiological events. New techniques for engineering cardiac tissue allow unprecedented means of modeling these phenomena in vitro. However, experimental design is often hampered by a lack of models that can be adapted to the ideal conditions these methods allow. To address these deficiencies, we developed a mathematical model to calculate the distribution of stress and strain in fibrous cardiac tissue. The fluid-fiber-collagen model characterizes the mechanical behavior of cardiac tissue and is solved analytically for the distributions of stress and strain along the myocardial fibers. An example application of the model is presented: modeling the distribution of strains in the vicinity of an ischemic region. The ischemic region is stretched during systole, as has been shown in previous one-dimensional models. Our model predicts a complex distribution of stretch in the border zone surrounding the ischemic region and in nonischemic regions surrounding the border zone. These strain patterns may predict patterns of mechanochemical coupling that results in localized fibrosis, altered gene expression, or the mechanoelectrical signaling events that potentiate cardiac arrhythmias.
Department of Physics and Astronomy, Vanderbilt University, Nashville, Tennessee 48309, USA.
David C
DC
Latimer
Bradley J
BJ
Roth
Kevin Kit
KK
Parker
D001145:Arrhythmias, Cardiac / Q000209:etiology; D003094:Collagen; D005355:Fibrosis; D005786:Gene Expression Regulation; D006801:Humans; D006874:Hydrostatic Pressure; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology*; D017202:Myocardial Ischemia / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D013314:Stress, Mechanical; D013599:Systole; D023822:Tissue Engineering / Q000379:methods*
D003094:Collagen