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1 Cardiovascular Division, Veterans Affairs Medical Center, and University of Utah Health Sciences Center, Salt Lake City, Utah 84132; and 2 Cardiovascular Section, University Heart Center and Veterans Affairs Medical Center, Tucson, Arizona 85723
Loss of the positive
force-frequency relationship is a characteristic finding in failing
hearts. The mechanisms of this change are not well understood.
Myocardial infarction (MI) was induced in rabbits to produce left
ventricular (LV) dysfunction. Beginning 1 day after MI, a subgroup of
rabbits received diiodothyropropionic acid (DITPA) (3.75 mg · kg
1 · day1
sc) for 3 wk. We measured contractions, Ca2+ transients,
action potentials, and sarcoplasmic reticulum (SR) Ca2+
content at different stimulation rates in single LV myocytes. The
shortening-frequency relationship was markedly flattened in MI myocytes
compared with control myocytes. In addition, Ca2+
transients, action potentials, and contractions were prolonged. Myocytes from DITPA-treated MI rabbits had preserved inotropic responses to increased stimulation rate and normal duration of action
potentials and Ca2+ transients. SR Ca2+ content
increased significantly when stimulation rate was increased from 0.5 to
2.0 Hz in control myocytes but did not change significantly in MI
myocytes. Myocytes from DITPA-treated MI rabbits had a greater frequency-dependent increase in SR Ca2+ content compared
with the untreated MI rabbits. Thus single myocytes from infarcted
rabbit hearts have frequency-dependent abnormalities of contractility,
Ca2+ cycling, and action potential repolarization. The
flattened contraction-frequency relationship can be partially explained
by an attenuation of the normal enhancement of SR Ca2+
content that occurs when stimulation rate is increased. Chronic DITPA
administration after MI largely prevents the development of these abnormalities.
myocardial infarction; calcium; ion channels; congestive heart failure; sarcoplasmic reticulum; rabbit; contractility; thyroid hormone; diiodothyropropionic acid
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