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Ann Thorac Surg 1998;66:1618-1625
© 1998 The Society of Thoracic Surgeons

Triiodothyronine reverses depressed contractile performance after excessive catecholamine stimulation

^a Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany

Accepted for publication May 11, 1998.

Address reprint requests to Dr Vahl, Chirurgische Klinik, Abt Herzchirurgie, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany

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°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).

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