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Pressure-calcium relationships in perfused mouse hearts

¹Cardiovascular Institute and ²Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania; ³Department of Cardiology at Freeman Hospital and ⁴University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom

Submitted 13 September 2005 ; accepted in final form 10 January 2006

We explored the relationship between left ventricular (LV) pressure and intracellular free calcium concentration ([Ca]_i) in the isolated perfused mouse heart. [Ca]_i (rhod-2) and LV pressure were recorded simultaneously. In response to increases in LV volume (Frank-Starling, FS, protocol), there were increases in developed pressure (up to 250%), with no changes in pressure morphology (rise or relaxation time) or [Ca]_i (magnitude and morphology) for up to 10 min. During transient increases in the stimulus interval at a fixed LV volume (mechanical restitution, MR, protocol), developed pressure increased significantly (31.3 ± 1.2%), with relatively small changes in peak systolic [Ca]_i (7.4 ± 1.4%). The relaxation of [Ca]_i, however, was prolonged (30.0 ± 5.5%), resulting in prolonged pressure relaxation (21.2 ± 1.9%) and increased area under the calcium transient that paralleled the increase in developed pressure (1:1 ratio). A model-based analysis showed that changes in LV pressure during the MR protocol could be completely explained by altered [Ca]_i; it was not necessary to invoke any changes in model parameters (i.e., dynamic processes that link calcium to pressure). For the FS data, the model predicted only a change in the gain parameter; however, this change alone cannot reproduce well-established length-dependent changes in the steady-state force-pCa relationship. In summary, the mouse myocardium appears to be unique in that significant changes in peak developed pressure can occur with little or no change in the peak [Ca]_i. Additionally, unlike other mammalian species, load-dependent prolongation of pressure relaxation is absent in the mouse heart, and pressure relaxation is primarily governed by intracellular free calcium relaxation.

murine heart; length-dependent activation; load-dependent relaxation; excitation-contraction coupling; model-based analysis

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