Background:The “euthyroid sick syndrome” may intensify dysfunction of the heart during acute myocardial ischemia. The present research was undertaken to outline the effects of preischemic short-term triiodothyronine (T[sub]3[/sub]) administration on hemodynamic function and metabolism of the myocardium during reperfusion.Material/Methods: Thirty-six isolated working rat hearts were assigned to three experimental groups and a control group. The hearts were removed from the animals and perfused in the modified Langendorff model. They were subjected to 30 minutes of initial perfusion, 40 minutes of ischemia, and 15 minutes of reperfusion. The experimental groups received 10 extra minutes of T[sub]3[/sub] administration followed by initial perfusion (concentration of T[sub]3[/sub] was: group 1–5.4 pmol/l, group 2–27 pmol/l, and group 3–54 pmol/l). Control hearts received perfusate without T[sub]3[/sub]. We evaluated the postischemic recovery of left ventricular function (aortic pressures, heart rate, cardiac output), coronary flow, and oxygen consumption.Results: Progressive percentage of recovery of aortic systolic pressure, aortic mean pressure, and cardiac output with increasing concentration of T[sub]3[/sub] was observed. Cardiac output reached the best recovery in the group with the highest concentration of T[sub]3[/sub] (80.9±7.5%) and was significantly better in comparison with the control group and the other experimental groups. No significant differences in coronary flow and oxygen consumption were noted.Conclusions: Triiodothyronine administered before ischemia improves postischemic left ventricular function with no changes in oxygen consumption and coronary flow.

Keywords: Triiodothyronine - administration & dosage, Coronary Circulation - drug effects, Coronary Vessels - drug effects, Heart - physiology, Hemodynamics - drug effects, Myocardial Ischemia - metabolism, Myocardium - metabolism, Oxygen - metabolism, Oxygen Consumption - drug effects, Reperfusion, Time Factors, Triiodothyronine - pharmacology