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Monophasic action potential (MAP) measurements have been used to characterize the in vivo electrophysiology of the heart. The extension of this technique to the murine heart has raised questions about the sources underlying the MAP and the effect of tissue properties on the time course and amplitude of the MAP. A 3D bidomain model of the murine right ventricular free wall with adjoining endo and epicardial baths and realistic channel dynamics was constructed to study the genesis of MAP signals in small hearts due to pressure contact. In this study, the degree of tissue compression, fi, under the electrode was varied to determine the effect on amplitude (MAPA) and duration (MAPD) of the MAP relative to the underlying transmembrane action potential (TAP). Increasing fi by 40% more than doubled the amplitude and reduced the error between the MAPD and TAPD. These results indicate that reducing the length constant (and increasing spatial gradients) under the MAP electrode improves the MAP/TAP correlation.