AJP - Heart and Circulatory Physiology, Vol 254, Issue 2 265-H273, Copyright © 1988 by American Physiological Society
T3 treatment does not prevent myocardial dysfunction in chronically diabetic rats
R. W. Barbee, R. E. Shepherd and A. H. Burns
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
The isolated working heart preparation was used to investigate the effect
of continuous triiodothyronine (T3) administration on cardiac function and
metabolism of rats rendered diabetic for a period of 4 wk with streptozocin
(STZ). T3 controlled-release pellets were implanted 1 wk after STZ (70
mg/kg) injection. Rats injected with citrate buffer without STZ received T3
pellets 1 and/or 2 wk later. A comparable number of rats received placebo
pellets. Untreated diabetic rats exhibited a decrease in spontaneous heart
rate and myocardial cytochrome c concentrations concurrent with depressed
plasma T3 values compared with untreated controls. T3 treatment did not
improve in vitro cardiac performance (assessed as cardiac output times peak
systolic pressure per gram dry heart weight) in hearts from diabetic rats
perfused with glucose alone. Addition of octanoate reversed this depression
and improved cardiac function to a greater extent in treated than in
untreated diabetic animals. However, these differences between treated and
untreated diabetic animals disappeared when heart rate was controlled by
cardiac pacing. Furthermore, T3 treatment of controls and diabetics did not
alter the oxidation of octanoate or the cardiac responsiveness to
isoproterenol. These results suggest that experimental diabetic
cardiomyopathy is partly attributable to a substrate deficiency and is not
due entirely to hypothyroidism.
