Abstract
We investigated the formation of a “nonthyroidal illness” (NTI) in pigs undergoing
ventricular fibrillation (VF) and resuscitation. Seven minutes after VF twenty-one
pigs received either Epinephrine (E: 45 µg/kg B.W.; n = 7), Norepinephrine (NE: 45
µg/kg B.W.; n = 7), or Vasopressin (VP: 0.8 U/kg B.W.; n = 7). We determined the serum
concentrations (sc) of total T4 (TT4), FT4, total T3 (TT3) and rT3 120 min before, during (t0), and 5, 15, 60 and 120 min after VF. At the end of the observation period we figured
out the in-vitro T3-generation (kM, Vmax), the in-vitro rT3-generation, the in-vitro rT3-decomposition (kM, Vmax) and the content of cytosolic sulfhydryls (total sulfhydryls, non-protein bound sulfhydryls)
in liver and kidney specimen. Animals not undergoing VF served as controls (C) for
parameters measured in the intracellular compartment. TT4- and TT3-sc decreased to 3.3 ± 0.6 µg/dl (p < 0.05, vs. t0) and 15.2 ± 4.1 ng/dl (p < 0.05, vs t0), resp. FT4-sc remained stable for five minutes (2.63 ± 0.41 ng/dl) before declining to 1.8 ±
0.39 ng/dl (p < 0.05, vs. t0). The rT3-sc raised finally to 46.9 ± 7.3 ng/dl (p < 0.05, vs t0). Iodothyronine sc did not exhibit differences between E-, NE- and VP-treatment.
Neither in-vitro T3-generation, nor in-vitro rT3-generation, nor in-vitro rT3-decomposition nor intracellular sulfhydryl content were affected by the events of
VF and resuscitation as compared to the controls. We therefore conclude that i. A
low T3 high rT3-syndrome is developed 120 min after VF in pigs; ii. The 5′-deiodination in liver
and kidney, which contributes by approximately 60% to circulating T3 in euthyroid healthy beings, does not account for the alterations of iodothyronine
sc within this interval of time.
Key words
Resuscitation - rT3
- Cardiac Arrest - FT4
- Non Thyroid Illness - Equilibrium Dialysis - 5′-Deiodination - Vasopressin - 5-Deiodination
- Catecholamines