NOVEL ACTIONS OF THYROID-HORMONE - THE ROLE OF TRIIODOTHYRONINE IN CARDIAC TRANSPLANTATION

In clinical heart transplantation, the heart is procured from brain de ad (ED) organ donors who acutely experienced a variety of critical ill nesses. In all of these conditions, a profound derangement of the thyr oid profile has been observed. Although the plasma levels of thyroid s timulating hormone (TSH) remain unchanged, there is a rapid decline in free triiodothyronine (FT3) levels (P < 0.0001) as well as an elevati on of reverse triiodothyronine (rT(3)) (P < 0.001). Following inductio n of experimental brain death, the heart exhibits a progressive signif icant hemodynamic-biochemical deterioration (reduction of cardiac cont ractility, depletion of high energy phosphates, glycogen, and accumula tion of tissue lactate). The administration of T-3 to ED animals resul ted in rapid reversal of the hemodynamic and metabolic derangements. T he impact of T-3 therapy to unstable human brain dead organ donors has resulted in rapid hemodynamic stability allowing significant reductio n of inotropic support (P < 0.001). These hearts, following cardiac tr ansplantation, exhibited excellent hemodynamic function in the recipie nts. The low FT3 state has also been observed during and following ope n heart surgery on cardiopulmonary bypass (CPB). Therefore, at the com pletion of the heart transplant procedure, T-3 was also administered t o the recipient to prevent relapse of the hemodynamic-metabolic abnorm ality observed in the donor. The impact of T-3 therapy to initially un stable donors allowed for rapid inotropic reduction and recovery of th e heart, thus enlarging the donor organ pool and improving the outcome of the recipients following cardiac transplantation.