title: Pressure-calcium relationships in perfused mouse hearts.
abstract: 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.
authors.affiliation: Cardiovascular Institute, University of Pittsburgh, 749 Benedum Hall, Pittsburgh, PA 15261, USA.
authors.forename: Guy A
authors.initials: GA
authors.lastname: MacGowan
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Kirk
authors.forename: Caroline
authors.initials: C
authors.lastname: Evans
authors.forename: Sanjeev G
authors.initials: SG
authors.lastname: Shroff
mesh_terms: D000465:Algorithms; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002118:Calcium / Q000097:blood / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006575:Heterocyclic Compounds, 3-Ring; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology; D013050:Spectrometry, Fluorescence; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D006575:Heterocyclic Compounds, 3-Ring; C068483:rhod-2; D002118:Calcium