EFFECT OF TRIIODOTHYRONINE ON POSTISCHEMIC MYOCARDIAL-FUNCTION IN THE ISOLATED HEART

Thyroid dysfunction has been shown to have a significant impact on hemodynamic status and cardiac function. The purpose of this study was to determine the influence of triiodothyronine (T-3) on cardiac functional recovery after ischemia in a dose-dependent manner. Postischemic functional recovery was assessed in isolated rabbit hearts mounted in a modified Langendorff preparation. Left ventricular systolic, diastolic, and peak developed pressures were measured before and after ischemia, and calculated as a percentage of preischemic function. Two cohorts of hearts were studied: the first was exposed to warm ischemia until a myocardial contracture of 4 mm Hg was produced; the second cohort was exposed to warm ischemia until a contracture of 15 mm Hg was observed. In each cohort, T-3 was added to the perfusion solution after ischemia in a physiologic concentration (2.5 x 10(-9) g/mL; 1 x T-3), as well as ten times (2.5 x 10(-8) g/mL; 10 x T-3) and a hundred times (2.5 x 10(-7) g/mL; 100 x T-3) the physiologic concentration. One group, given the carrier only but without T-3, served as the control. Rabbit hearts exposed to a short period of ischemia (4-mm Hg diastolic contracture) showed increased recovery with 1 x T-3 and 10 x T-3. 100 x T-3 did not bring about improved left ventricular recovery versus that in the control group. Rabbit hearts in the 15 mm Hg-diastolic contracture cohort showed increased recovery with 10 x T-3 but not with 1 x T-3. 100 x T-3 led to decreased recovery in this cohort versus that in the control group. T-3 supplementation had no influence either on the wet-dry weight ratio of myocardium, measured at the end of reperfusion, or on coronary flow throughout the postischemic period. These findings indicate that T-3 enhances recovery after ischemia in a relatively dose-dependent fashion over a wide therapeutic range.