Thyroid hormone treatment in brain dead organ donors has been extensively studied and applied in the clinical setting. However, its effectiveness remains controversial due to a varying degree of success and a lack of knowledge about the therapeutic effects of 3,3',5-triiodo-l-thyronine (T3). T3 pre-conditioning leads to anti-apoptotic and pro-mitotic effects in liver tissue following ischemia/reperfusion injury. Therefore, we aimed to study the effects of T3 pre-conditioning in the liver of brain dead rats.

Brain death (BD) was induced in mechanically ventilated rats by inflation of a Fogarty catheter in the epidural space. T3 (0.1 mg/Kg) or vehicle was administered intraperitoneally 2 hrs prior to BD induction. After 4 hrs of BD, serum and liver tissue were collected. RT-qPCR, routine biochemistry, and immunohistochemistry were performed.

Brain dead animals treated with T3 had lower plasma levels of ASAT and ALAT, reduced BAX gene expression, and less hepatic Caspase-3 activation and HO-1 expression compared to brain-dead animals treated with vehicle. Interestingly, no differences in the expression of inflammatory genes (IL-6, MCP-1, IL-1b and TNF-a) or the presence of pro-mitotic markers (Cyclin-D and Ki-67) were found in brain dead animals treated with T3 compared to vehicle-treated animals.

T3 pre-conditioning leads to beneficial effects in the liver of brain dead rats, as seen by lower cellular injury, reduced apoptosis and less oxidative stress, and suggests an important role for T3 hormone therapy in the management of brain dead donors.

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