| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cardiovascular Institute, University of Pittsburgh, Pittsburgh, PA, USA; Department of Cardiology, Freeman Hospital, Newcastle upon Tyne, United Kingdom; University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom
2 Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: sshroff{at}pitt.edu.
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 minutes. 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 which 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.
This article has been cited by other articles:
|
|
 |
|
  K. B. Campbell, A. M. Simpson, S. G. Campbell, H. L. Granzier, and B. K. Slinker Dynamic left ventricular elastance: a model for integrating cardiac muscle contraction into ventricular pressure-volume relationships J Appl Physiol, April 1, 2008; 104(4): 958 - 975. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. H. Talukder, A. Kalyanasundaram, L. Zuo, M. Velayutham, Y. Nishijima, M. Periasamy, and J. L. Zweier Is reduced SERCA2a expression detrimental or beneficial to postischemic cardiac function and injury? Evidence from heterozygous SERCA2a knockout mice Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1426 - H1434. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. H. Talukder, A. Kalyanasundaram, X. Zhao, L. Zuo, P. Bhupathy, G. J. Babu, A. J. Cardounel, M. Periasamy, and J. L. Zweier Expression of SERCA isoform with faster Ca2+ transport properties improves postischemic cardiac function and Ca2+ handling and decreases myocardial infarction Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2418 - H2428. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Liu, R. B. Marchase, and J. C. Chatham Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1391 - H1399. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Diolez, V. Deschodt-Arsac, G. Raffard, C. Simon, P. D. Santos, E. Thiaudiere, L. Arsac, and J.-M. Franconi Modular regulation analysis of heart contraction: application to in situ demonstration of a direct mitochondrial activation by calcium in beating heart Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R13 - R19. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
