Modelling and measuring electromechanical coupling in the rat heart.

Tension-dependent binding of Ca(2+) to troponin C in the cardiac myocyte has been shown to play an important role in the regulation of Ca(2+) and the activation of tension development. The significance of this regulatory mechanism is quantified experimentally by the quantity of Ca(2+) released following a rapid change in the muscle length. Using a computational, coupled, electromechanics cell model, we have confirmed that the tension dependence of Ca(2+) binding to troponin C, rather than cross-bridge kinetics or the rate of Ca(2+) uptake by the sarcoplasmic reticulum, determines the quantity of Ca(2+) released following a length step. This cell model has been successfully applied in a continuum model of the papillary muscle to analyse experimental data, suggesting the tension-dependent binding of Ca(2+) to troponin C as the likely pathway through which the effects of localized impaired tension generation alter the Ca(2+) transient. These experimental results are qualitatively reproduced using a three-dimensional coupled electromechanics model. Furthermore, the model predicts that changes in the Ca(2+) transient in the viable myocardium surrounding the impaired region are amplified in the absence of tension-dependent binding of Ca(2+) to troponin C.