Triiodothyronine therapy for heart donor and recipient

Abstract

Both (1) brain-dead donors and (2) transplant recipients on cardiopulmonary bypass suffer a depletion in plasma-free triiodothyronine (T3), which leads to metabolic changes (from inhibition of mitochondrial function), resulting in myocardial energy store depletion. Replacement therapy with T3 reverses these changes in both donor and recipient. Donor heart energy stores and function will be maintained at optimum levels if T3 therapy is administered to both donor and recipient at the time of transplantation.