The term rT3 refers to a form of tri-iodo-thyronine, one of the active iodinated thyroid hormone. Thyroid hormones are made by the thyroid gland. Thyroid hormones have long been recognized to regulate metabolism (energy activity) of cells. Thyroid hormones are iodinated (the reason why iodine is important for our diet), usually coming from sea salt. There are two forms of iodinated thyroid hormones: T3 and T4. These respectively contain two iodines and three iodines. T3 has several forms, depending on where the iodine attaches to the hormone. One of these is rT3. Cells contain a variety of iodeinases (enzymes that remove iodines).
Thyroid hormones are quite hydrophobic (i.e. do not dissolve well in water) and dissolve quite readily in membranes. In order for thyroid to be distributed in blood, they must be bound by carrier proteins. Protein-bound T3 and T4 are carried to the cells where the molecules dissolve into membranes and then act on intracellular receptors located in the cell nuclei. Apparently, the presence of thyroid hormones also increase the stiffness (rigidity) of membranes. Hurlburt (2000) has proposed that thyroid hormones mediate their effects by influencing membrane rigidity and receptors.
For many years, TRH (thyrotropin release hormone – a pituary peptide that causes the release of thyrotropin, a hormone that stimulates the thyroid gland to make T3 and T4) has been reported to be neuroprotective in spinal cord injury. TRH and its analogs have diverse effects on the brain that cannot be readily explained by the effects of thyroid hormones. For example, high doses of TRH block opiate receptors and increase the excitability of the nervous system. The latter is particularly interesting because early spinal cord injury studies suggest that high doses of TRH can reverse anesthesia produced by pentobarbital and even gaseous anesthesia.
Regarding metabolism in the spinal cord, please understand that many of the early studies of metabolism in the spinal cord did not take into the account the death of many cells at the injury site. If 80% of the cells at the injury site dies, this is likely to produce very large declines in tissue metabolic activity. So, scientists need to normalize the metabolic activity to the number of living cells present at the injury site. Most scientists who have studied metabolic activity in injured spinal cords, however, did not measure the number of living cells in the tissue. That is one of the reasons why estimates of metabolic activity in injured spinal cords must be looked at with a grain of salt.
Little is known about the levels of thyroid hormones in injured spinal cords. Several studies have reported low levels of blood levels of T3 in people with spinal cord injury, however. Prakash (1983) and Bugaresti, et al. (1993) had reported that while serum T3 is low, serum rT3 is high in people with spinal cord injury. Bauman & Spungen (2000) likewise have reported that many people with spinal cord injury have low T3 levels and elevated rT3, attributing this to associated illness. They point out that the current practice is not to treat such thyroid abnormalities due to nonthyroid illness but suggests the application of “appropriate” interventions to correct these abnormalities “promises to improve longevity and quality of life of persons with SCI”.