In clinical
heart transplantation, the heart is procured from
brain dead (BD) organ donors who acutely experienced a variety of
critical illnesses. In all of these conditions, a profound derangement of the thyroid profile has been observed. Although the plasma levels of
thyroid stimulating hormone (TSH) remain unchanged, there is a rapid decline in free
triiodothyronine (FT3) levels (p < 0.0001) as well as an elevation of
reverse triiodothyronine (rT3) (p < 0.001). Following induction of experimental
brain death, the heart exhibits a progressive significant hemodynamic-biochemical deterioration (reduction of cardiac contractility, depletion of high energy
phosphates,
glycogen, and accumulation of tissue
lactate). The administration of T3 to BD animals resulted in rapid reversal of the hemodynamic and metabolic derangements. The impact of T3
therapy to unstable human
brain dead organ donors has resulted in rapid hemodynamic stability allowing significant reduction of inotropic support (p < 0.001). These hearts, following
cardiac transplantation, exhibited excellent hemodynamic function in the recipients. The low FT3 state has also been observed during and following open heart surgery on
cardiopulmonary bypass (CPB). Therefore, at the completion of the heart transplant procedure, T3 was also administered to the recipient to prevent relapse of the hemodynamic-metabolic abnormality observed in the donor. The impact of T3
therapy to initially unstable donors allowed for rapid inotropic reduction and recovery of the heart, thus enlarging the donor organ pool and improving the outcome of the recipients following
cardiac transplantation.