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Am J Physiol Heart Circ Physiol 273: H1432-H1439, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 273, Issue 3 1432-H1439, Copyright © 1997 by American Physiological Society

ARTICLES

Mitochondrial calcium content in isolated perfused heart: effects of inotropic stimulation

C. S. Moravec, R. W. Desnoyer, M. Milovanovic, M. D. Schluchter and M. Bond
Center for Anesthesiology Research, Cleveland Clinic Foundation, Ohio 44195, USA.

We tested the hypothesis that in the intact heart, mitochondrial metabolism is activated by mitochondrial Ca2+ uptake during increased work. We measured left ventricular pressure (LVP), pyruvate dehydrogenase (PDH) activity, and mitochondrial and A band elemental content by electron probe microanalysis (EPMA) in Langendorff-perfused hamster hearts under control conditions, after isoproterenol (10(-6) M) stimulation, and after increasing perfusion pressure from 60 to 100 mmHg. Hearts were rapidly frozen, then EPMA was performed on cryosections cut from the surface of the frozen hearts; PDH activity was measured from the same area. Isoproterenol and elevated perfusion pressure increased LVP by 185 +/- 21 and 58 +/- 14%, respectively, versus controls. PDH activity increased from 10.4 +/- 1.5 (mean +/- SE) nmol.min-1. mg protein-1 (controls) to 21.6 +/- 3.5 (isoproterenol) and 18.5 +/- 3.2 nmol.min-1.mg protein-1 (increased perfusion pressure). There was no significant change in mitochondrial Ca1 in response to isoproterenol [1.2 +/- 0.1 (mean +/- SE) mmol/kg dry wt] or increased perfusion pressure (1.1 +/- 0.1) versus controls (1.0 +/- 0.1). These results suggest that, in the intact heart, mechanisms other than mitochondrial Ca2+ uptake may contribute to PDH activation and increased cardiac work.


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