BACKGROUND Triiodothyronine (T3) administration can improve postischemic myocardial recovery. Heparin can interfere with cellular binding of T3. Introduction of heparin into an isolated heart model may interfere with this effect. METHODS Four groups of 8 rat hearts were placed on a modified Langendorff apparatus. All groups underwent 15 minutes of perfusion with modified Krebs-Henseleit solution (KH), followed by 20 minutes of normothermic global ischemia and 30 minutes of reperfusion. Group I underwent reperfusion with KH. Group II underwent reperfusion with KH and 1 x 10(-6) mol/L of T3. In group III, hearts underwent preischemic perfusion with heparinized KH (1,000 U/L) and reperfusion with KH containing 1 x 10(-6) mol/L of T3 and 1,000 U/L of heparin. In group IV, rats were given heparin at 2,000 IU/kg 30 minutes before sacrifice, and isolated hearts were reperfused with KH and 1 x 10(-6) mol/L of T3. A latex balloon in the left ventricle monitored hemodynamic variables. RESULTS Left ventricular developed pressure throughout postischemic reperfusion was greater in all the groups receiving T3 when compared with group I. Group II showed significantly greater recovery than either group III (p < 0.05) or group IV (p < 0.05). CONCLUSIONS Addition of T3 to the reperfusate enhances postischemic myocardial recovery in the isolated heart model, whereas addition of heparin reduces this effect.