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Articles in PresS, published online ahead of print December 6, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00466.2001
Submitted on May 30, 2001
Accepted on November 29, 2001
1 Biophysics Program and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA
2 Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, OH, USA
3 Department of Veterinary Biosciences, The Ohio State University, Columbus, OH, USA
4 Department of Food Science and Technology, The Ohio State University, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: altschuld.2{at}osu.edu.
We examined mechanical alternans and electromechanical restitution in normal and failing rat hearts. Alternans occurred at 5 Hz in failing vs 9 Hz in control hearts and was reversed by 300 nM isoproterenol, 6 mM extracellular Ca2+, 300 nM BayK 8644, or 50 nM ryanodine. Restitution curves comprised phase I, which was completed prior to 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 vs 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 (µ mM) plus ryanodine (200 nM) potentiated phase I to a significantly greater extent in control vs 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 SHHF rat heart.
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