R. Boado

Evidence suggesting that the sympathetic nervous system mediates thyroidal depression in turpentine-induced nonthyroidal illness syndrome.

Acute superior cervical ganglionectomy (SCGx) induces in the rat a supraliminal release of neurotransmitter in the innervated tissues (i.e., thyroid gland). This temporary adrenergic hyperactivity is correlated with a significant depression of the thyroid economy resembling the nonthyroidal illness (NTI) syndrome in the rat, and suggest that the sympathetic nervous system may mediate thyroidal changes in NTI. In order to gain further insight into the thyroidal depression in the NTI syndrome, we studied the thyroidal norepinephrine (NE) turnover in turpentine oil (TURP)-induced NTI syndrome and the role of the cervical ganglia (SCG) in the development of NTI in the rat. TURP administration to sham operated rats induced a rapid and significant fall in plasma T4 and TSH levels, in the thyroidal response to exogenous TSH (TIU) and in the thyroidal NE content compared to controls (sham + saline) (T4: 3.1 +/- 0.3 vs. 5.1 +/- 0.6 micrograms/dl, respectively, mean +/- SE, p less than 0.02; TSH: 1.4 +/- 0.4 vs. 4.7 +/- 1.4 ng/ml, respectively, p less than 0.05; TIU: 92 +/- 14 vs. 201 +/- 20 cpm.microliter thyroid/cpm.mg plasma (T/P ratio), respectively, p less than 0.01; thyroidal NE: 680 +/- 20 vs. 761 +/- 29 pg/mg thyroid, respectively, p less than 0.05). The thyroidal turnover rate of NE, however, was significantly increased in TURP-injected rats compared to controls (122 +/- 13 vs. 86 +/- 10 pg/mg/h, respectively, p less than 0.05). TURP injection to chronic SCGx rats induced a similar fall in plasma TSH compared to controls (SCGx + saline) (1.3 +/- 0.2 vs. 4.3 +/- 1.1 ng/ml, respectively, p less than 0.02); plasma T4 and TIU, however, did not change significantly (T4: 3.4 +/- 0.4 vs. 3.7 +/- 0.3 micrograms/dl, respectively, NS; TIU: 172 +/- 8 vs. 226 +/- 27 T/P ratio, respectively, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of diabetes, β-hydroxybutyric acid and metabolic acidosis on the pituitary-thyroid axis in the rat

Previous studies demonstrated alterations of thyroidal economy in untreated diabetes mellitus both in man and experimental animals. To test the role of β-hydroxybutyric acid (BHB) and acidosis in generating such changes, we studied the pituitary-thyroid axis of streptozotocin-diabetic rats, BHB or ammonium chloride (NH4CI)-treated normal rats. Serum TSH, pituitary content and pituitary concentration of TSH, serum T4, T3 and free T4 (FT4), were all measured by RIA. In short term (2 days) diabetic rats the pituitary content of TSH was normal whereas the concentration (per mg of protein) was elevated (p< 0.05 versus control group). Serum TSH (p< 0.05), serum T4 (p< 0.05), serum T3 (p<0.01) and serum FT4 (p<0.05) were all significantly decreased. In long term (30 days) untreated diabetic rats serum changes were similar to the short term diabetic group, though the pituitary content of TSH was significantly decreased (p< 0.05). Animals treated with NH4Cl had no variations from controls. However, rats treated with BHB displayed a significant decrease in pituitary content of TSH (p< 0.05), pituitary concentration of TSH (p< 0.05) and in plasmaTSH (p< 0.01 ), and normal thyroid hormones in serum. No significant changes were seen in theTSH response toTRH in 2 or 30 days untreated diabetic and in BHB — treated animals. The data suggest that BHB, although not NH4CI acidosis, may be capable of inducing a moderate depression of pituitary and plasma TSH of a lesser magnitude of that accompanying the full, long term diabetic state in the rat.

Reciprocal effects of an acute load of thyroxine or triiodothyronine on their peripheral metabolism and deiodination in the cold-acclimated rat

Wistar rats acclimated to cold received iv 25μg T4/100g bw, 21 μg T3/100g bw or 2.5 μg T3/100g bw, to observe the changes induced in the peripheral metabolism of 125I-T4 and 125I-T3 relative to cold-adapted untreated animals. Each animal was injected with a tracer dose of either labelled hormone in addition to the T4 or T3 load, and placed in metabolic cages for 24 hour collection of urine and feces. Sequential heparinized blood samples were obtained by cardiac puncture. A T4 load decreased the deiodination of 125I-T4 and 125I-T3 (p < 0.01) as revelated by urinary 125I. A T3 load, in the two dosages employed, decreased the deiodination of 125I-T3(p < 0.01) but had no effect on deiodination of 125I-T4. Similarly, a T4 load increased the fecal excretion of both radioactive iodothyronines (p < 0.01) whereas a T3 load failed to alter the excretion of 125I-T4. In cold-adapted animals plasma TSH was elevated (p < 0.05) and plasma T4 was low (p < 0.001) as compared to rats housed at 22 C. It is concluded that the relative contribution of T4 and T3 to the metabolic state in the rat is not significantly altered by cold exposure.