Abstract
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 × 10 −9 g/mL; 1 × T 3), as well as ten times (2.5 × 10 −8 g/ml; 10 × T 3 and a hundred times (2.5 × 10 −7 g/mL; 100 × 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 × T 3 and 10 × 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 × T 3 but not with 1 × T 3. 100 × 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.
Published Version
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