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      Evidence Suggesting that the Sympathetic Nervous System Mediates Thyroidal Depression in Turpentine-Induced Nonthyroidal Illness Syndrome


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          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 (NTT) 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 NT! syndrome, we studied the thyroidal norepinephrine (NE) turnover in turpentine oil (TURP)-induced NT syndrome and the role of the cervical ganglia (SCG) in the development of NΗ 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 (ΗU) and in the thyroidal NE content compared to controls (sham + saline) (T4: 3.1 ± 0.3 vs. 5.1 ± 0.6 µg/dl, respectively, mean ± SE, p < 0.02; TSH: 1.4 ± 0.4 vs. 4.7 ± 1.4 ng/ml, respectively, p < 0.05; ΗU: 92 ± 14vs 201 ± 20 cpm µl thyroid/cpm·mg plasma (T/P ratio), respectively, p < 0.01; thyroidal NE: 680 ± 20 vs. 761 ± 29 pg/mg thyroid, respectively, p < 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 < 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 < 0.02); plasma T4 and TIU, however, did not change significantly (T4: 3.4 ± 0.4 vs. 3.7 ± 0.3 µg/dl, respectively, NS; ΗU: 172 ± 8 vs. 226 ± 27 T/P ratio, respectively, NS). Denervation of thyroid gland by sectioning of the external carotid nerve (ECNx) also blocked the fall in ΗU induced by TURP; on the other hand, a section of the internal carotid nerve (ICNx) (which does not innervate the thyroid gland) failed to prevent TURP effect on TIU (T/P ratio: sham + saline, 359 ± 58 vs. sham + TURP, 190 ± 23, p < 0.025; ECNx + saline, 266 ± 42 vs. ECNx + TURP, 274 ± 39, NS; ICNx + saline, 290 ± 57 vs. ICNx + TURP, 152 ± 29, p < 0.02). Our data suggest that (1) the NΠ is associated with an increase of the thyroidal NE turnover; (2) the SNS mediates the fall in plasma T4 and inTIU observed in NΠ syndrome through changes in the activity of the SCG, and (3) TSH fall in NΠ appears to be unrelated to SCG activity.

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          Author and article information

          S. Karger AG
          04 April 2008
          : 53
          : 4
          : 360-364
          Laboratorio de Investigaciones Endocrinologicas, Hospital de Clínicas and Catedra de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Argentina
          125742 Neuroendocrinology 1991;53:360–364
          © 1991 S. Karger AG, Basel

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          : 12 June 1990
          : 17 September 1990
          Page count
          Pages: 5
          Original Paper

          Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
          Thyroid,Superior cervical ganglia,Nonthyroidal illness syndrome


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