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Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21205
Mechanoelectric
coupling in the heart is well documented and has been suggested as a
cause of arrhythmia. One hypothesized mechanism for the stretch
sensitivity of cardiac muscle is the presence of stretch-activated
channels (SACs). This study uses modeling to explore the influence of
SACs on cardiac resting potential, excitation threshold, and action
potential in the context of arrhythmia. We added a putative SAC,
modeled as a linear, time-independent conductance with reversal
potential of 
20 or 50 mV, to guinea pig and frog
ventricular membrane models. Increased stretch conductance led to
resting potential depolarization, a decreased excitation threshold,
altered action potential duration, and, under certain conditions, early
afterdepolarizations. We conclude that stretch increases cellular
excitability, making the heart prone to ectopic activity. Regional
effects of stretch on action potential duration can vary and are
influenced by factors such as the SAC reversal potential, ionic
conditions, and baseline currents, all of which may lead to an
increased dispersion of refractoriness throughout the heart and
therefore an increased risk of arrhythmia.
mechanoelectric coupling; electrical stimulation; cardiac myocytes; stretch-activated channels; mathematical model
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