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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/H2614    most recent 00979.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by MacGowan, G. A. Articles by Shroff, S. G. Search for Related Content PubMed PubMed Citation Articles by MacGowan, G. A. Articles by Shroff, S. G.

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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