Novitzky D
University of South Florida, Tampa 33612, USA.
Thyroid. 1996 Oct;6(5):531-6. doi: 10.1089/thy.1996.6.531.
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.
在临床心脏移植中，心脏取自脑死亡（BD）器官捐献者，这些捐献者急性经历了各种危重病。在所有这些情况下，均观察到甲状腺指标的严重紊乱。尽管促甲状腺激素（TSH）的血浆水平保持不变，但游离三碘甲状腺原氨酸（FT3）水平迅速下降（p<0.0001），同时反三碘甲状腺原氨酸（rT3）升高（p<0.001）。诱导实验性脑死亡后，心脏表现出进行性显著的血流动力学-生化恶化（心脏收缩力降低、高能磷酸盐耗竭、糖原减少以及组织乳酸积累）。给脑死亡动物施用T3可迅速逆转血流动力学和代谢紊乱。T3治疗对不稳定的人脑死亡器官捐献者的影响导致血流动力学迅速稳定，从而显著减少了强心支持（p<0.001）。这些心脏在心脏移植后，在受者体内表现出良好的血流动力学功能。在体外循环（CPB）心脏直视手术期间及术后也观察到低FT3状态。因此，在心脏移植手术完成时，也给受者施用T3，以防止在供体中观察到的血流动力学-代谢异常复发。T3治疗对最初不稳定的供体的影响使得强心药物用量迅速减少且心脏恢复，从而扩大了供体器官库并改善了心脏移植后受者的预后。
