BACKGROUND: Conflicting results have been reported regarding the acute effects 
of triiodothyronine (T3) on myocardial contractile performance. The present 
study analyzes the role of T3 in reversing the depressant effect of excessive 
catecholamine stimulation in isolated porcine left ventricular myocardium.
METHODS: Thirty-six left ventricular trabeculae (0.4 x 6.0 mm) obtained from 6 
pigs were used for measurements of isometric force development, isotonic 
shortening, and intracellular calcium in three experimental series (measurement 
conditions: 37 degrees C; optimal length; supramaximal electrical stimulation, 1 
Hz; calcium measurement, fura-2 ratio method; frequency, 225 Hz). In series 1, 
isometric force development was measured before and after a 60-minute incubation 
with 10(-7) mol/L epinephrine in preparations with (n = 6) and without (n = 6) 
preceding fura-2 loading for calcium measurements. In series 2, the acute 
effects of a 30-minute administration of T3 (10(-9) mol/L) on isometric force 
and intracellular calcium were analyzed (n = 6). In series 3, after simultaneous 
fura-2 loading and a 6-hour 10(-7) mol/L epinephrine exposure the effects of T3 
(10(-9) mol/L, 30 minutes) on force development, shortening, and intracellular 
calcium transient were analyzed.
RESULTS: Long-term and high-dose epinephrine exposure induced a severe 
contractile depression with a significant reduction of isometric force 
development (p < 0.05) and increased diastolic (p < 0.001) and systolic calcium 
(p < 0.001). In normal porcine myocardium T3 had no effect on the extent of 
isometric force generation but accelerated the time course of force development 
(p < 0.05) and increased the calcium transient (p < 0.001). After induction of 
myocardial depression by epinephrine exposure T3 accelerated the intracellular 
calcium transients and reduced diastolic calcium. Triiodothyronine increased the 
shortening amplitude and the force amplitude (p < 0.01).
CONCLUSIONS: Triiodothyronine reverses depressed contractile performance after 
preceding high-dose epinephrine exposure in isolated porcine myocardium. 
Increased force amplitudes and unaltered or even reduced intracellular calcium 
transients argue in favor of a resensitization of the contractile apparatus for 
calcium by T3. The study supports a potential role for T3 treatment in depressed 
myocardium after previous excessive catecholamine exposure (eg, brain death, 
catecholamine treatment, ischemia).