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Am J Physiol Heart Circ Physiol 282: H1320-H1326, 2002. First published December 6, 2001; doi:10.1152/ajpheart.00466.2001
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Vol. 282, Issue 4, H1320-H1326, April 2002

Mechanical alternans and restitution in failing SHHF rat left ventricles

Cristian Dumitrescu1, Prakash Narayan1, Igor R. Efimov2, Yuanna Cheng2, M. Judith Radin4, Sylvia A. McCune3, and Ruth A. Altschuld1

1 The Ohio State University Biophysics Program and Dorothy M. Davis Heart and Lung Research Institute, Columbus 43210; 2 The Cleveland Clinic Foundation, Department of Cardiology, Cleveland 44195; 3 Department of Food Science and Technology and 4 Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio 43210

We examined mechanical alternans and electromechanical restitution in normal and failing rat hearts. Alternans occurred at 5 Hz in failing versus 9 Hz in control hearts and was reversed by 300 nM isoproterenol, 6 mM extracellular Ca2+, 300 nM -BAY K 8644, or 50 nM ryanodine. Restitution curves comprised phase I, which was completed before relaxation of the steady-state beat, and phase II, which occurred later. Phase I action potential area and developed pressure ratios were significantly reduced in the failing versus control hearts. Phase II was a monoexponential increase in relative developed pressure as the extrasystolic interval was increased. The plateau of phase II was significantly elevated in failing hearts. Thapsigargin (3 µM) plus ryanodine (200 nM) potentiated phase I to a significantly greater extent in control versus failing hearts and abolished phase II in both groups. The results suggest that both regulation of Ca2+ influx across the sarcolemma and Ca2+ release by the sarcoplasmic reticulum may contribute to altered excitation-contraction coupling in the failing spontaneously hypertensive heart failure prone rat heart.

heart failure; calmodulin; sarcoplasmic reticulum; calcium current facilitation


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