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The results of 11 experiments in a total of 571 rats (initial body weight of 150-250 g) are reported and some findings differing from those by others are discussed. It was repeatedly found that the animals after bilateral or even unilateral superior cervical sympathetic gangliectomy (GX) did not gain body weight during the first week after surgery. Though they started to grow later, for several weeks their body weight remained significantly less than that of sham operated controls (SH). Though such phenomenon has not yet been described, it may well explain the increase of thyroid weight (as expressed per body weight) after gangliectomy alone or combined with antithyroid drug treatment or hypophysectomy as described by others. It was suggested that such changes may depend on general metabolic changes resulting in a striking inhibition of body weight gain rather than on some specific effect of GX on the thyroid. This view was supported by evaluating the data on absolute and relative thyroid weight from 4 experiments in a total of 265 animals. The level of thyroxine (T4) and thyrotropic hormone (TSG) was repeatedly found to be significantly decreased after GX for until about 72 h and 24 h after surgery, respectively, which was in agreement with the data reported by others. However, the onset of such decrease was repeatedly found to appear at 6 or 8 h after surgery (in one experiment even at 3 h after surgery) which is also contrasting to the onset of T4 decrease at 14 h after surgery as found by others who suggested a correlation of such thyroid depression with a depletion of noradrenaline from the thyroid and may be even from median eminence. In these experiments, however, a decrease of T4 level was found several hours before the depletion of noradrenaline from the thyroid which appeared at 12 h after surgery and remained at similar level until 40 days, while no remarkable changes of that were found in SH animals (with the excretion of slight increase after 24 h). Between about 4 and 40 days after surgery no significant changes in T4 and TSH levels after GX were found as compared with SH animals is in agreement with others.4+n one experiment the increase of T4 at 2 h after TRH injection, resulting apparently from the effect of endogenous TSH, was significantly inhibited in GX animals at 8 days after surgery, while in other experiments (at 8 and 40 days after surgery) no difference in T4 level increase was found in GX animals as compared with SH ones. In general, it may be suggested that superior cervical sympathetic gangliectomy may result in some temporary and perhaps transient changes in pituitary-thyroid function in rats.

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Thyrotropin (TSH) levels in plasma were estimated with the aid of immunoradiometric assay in two groups of healthy male subjects aged 21-22 years in two experiments: 1. acute (30 min) exposure to 4 degrees C in a cold room; 2. insulin (0.01 U per kg i.v.) hypoglycemia at room temperature and at 55 degrees C. Immediately after cold exposure a decrease of TSH level was found (P less than 0.01), while no changes were observed during 30 min exposure. After insulin injection a significant decrease (P less than 0.05 to less than 0.001) of TSH level was found at 45 to 120 min irrespectively of the ambient temperature. In addition, increased levels of noradrenaline and decreased levels of growth hormone after cold exposure are presented.

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The disappearance of loading doses of thyroxine (T4) (100-20 000 microng T4 iv per rat weighing about 400 g) was measured with the aid of new technique allowing frequent blood sampling with maintenance of isovolaemia in anaesthetized animals. It was found that as early as 2 min after the injection more than half of the administered dose disappeared from the blood, while after 300 min only about 2% of that remained in the plasma. The direct relationship between the administered dose of T4 and both the relative and absolute level of free dialyzable T4 as well as of per cent of T4 displaced from plasma by sodium salicylate in vivo was demonstrated. Moreover, it was found that about 60% of administratered T4 is excreted by the bile within 300 min irrespective of the dose given, about 15 and 50% of that being found in the small intestine after 15 and 180 min, respectively. When two loading doses of T4 were subsequently administered and labelled with different isotopes, the amount of T4 from the first dose excreted by the bile was proportional to the amount of T4 from a second dose administered 18 h later. From all these observations it was concluded that, in vivo, an effective system for removal of the loading doses of thyroxine from the blood exists, and is presumably located in rapidly equilibrating tissues, mainly in the liver. From this point of view it appears that plasma protein carriers play an important role in the whole body economy of thyroxine, namely by maintaining a certain level in the blood to cover the actual functional needs of peripheral tissues.

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Comparison of Preventive Effect of T3 and T4 on Thyroxine Release from Thyroid Induced by Endogenous TSH after TRH Injection. Endocrinologia Experimentalis 11, 91-98, 1977. The technique of frequent blood sampling through polyethylene tubings inserted into blood vessels while maintaining isovolemia was used in pentobarbiturate anaesthetized rats weighing 250--300 g. The animals were fed low iodine diet for 4 weeks and injected 125I- (5 microgram Ci per animal daily) for 6 days begining from 8th day before the experiment. The effect of 25 microgram TRH injected through a cannula inserted into carotid artery in cranial direction was evaluated as per cent increase of labelled thyroxine in plasma at 120 min after the injection compared to its level at 30 min. Moreover, the inhibitory effect of various doses of thyroxine (T4; 5, 20 and 80 nmol kg-1) and triiodothyronine (T3; 1.25 and 5 nmol kg-1) injected i.v. at the intervals of 10, 20, 30, 60 and 180 min prior to TRH was investigated. It was found that the effect was time dependent, being negligible after 10 or 20 min, while after 60 and 180 min the increase of labelled T4 after TRH was fully prevented by 20 and 80 nmol T4 kg-1 and by 5 nmol T3 kg-1. The other doses (i. e. 5 nmol T4 kg-1 and 1.25 nmol T3 kg-1) were without effect. Thus, T3 was found to be significantly more active than equimolar doses of T4.

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Male rats of a final weight 350-400 g were fed low iodine diet for 4 weeks and injected radioiodide for 6 days prior to the experiment. They were anesthetized with pentobarbiturate and external arteriovenous shunt was made with the aid of thin polyethylene tubing to collect frequent blood samples while maintaining isovolemia as previously described. The injection of 20 mug synthetic TRH into carotic artery in rostral direction resulted in an increase of plasma thyroxine radioactivity showing a maximum at 120 min after the injection. This increase was prevented with the aid of i.v. injection 20 mug L-thyroxine at 20-180 min before TRH administration. Moreover, the preventive effect of thyroxine was completely blocked by the i.v. injection of actinomycin D (0.8 mg/kg) 60 min before thyroxine, while the administration of cycloheximide (4 mg/kg), at the same time, was without effect. The mechanism of this phenomenon remains to be further elucidated.

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