Biomedical subjects

H Kokesová

Publications and source records attributed to H Kokesová.

7 recordsLinked to original sources

PubMed1978

Lesions of some central nervous structures result in altered pituitary-thyroid response to acute decrease of blood thyroid hormone level.

Eight groups (3--6 animals each) of rats weighing 350--400 g were subjected to electrolytic lesions of various parts of habenular, thalamic and hypothalamic areas of brain. On the 6th day after the lesion the level of blood thyroid hormone was acutely decreased with the aid of isovolemic exchange transfusion (IET) of thyroid hormone free blood suspension. The level of thyroxine (T4) in plasma was measured before and during 180 min after IET with the aid of specific radioimmunoassay and the changes of its post-transfusion level were evaluated. It was found that in three groups of animals bearing large bilateral lesions either in lateral ventral thalamus or in a central inferior thalamus the response of T4 level during the post-transfusion period is similar to that found in intact control groups from previous experiments. This consists in an increase of T4 level nearly to the initial value within about 120--150 min after IET. In contrast, there was only a slight post-transfusion increase of T4 level in one group with small central lesion in medial superior thalamus and no increase in two groups bilaterally lesioned in habenular area and in another two groups lesioned either in a central part of dorsal hypothalamus or in a central dorsal part of ventral basal hypothalamus. It was concluded that some parts of brain may be involved in managing the appropriate response of pituitary-thyroid axis to acute decrease of thyroid hormone level, no plausible explanation of the mechanism ofthe observed phenomena being offered.

Animals↗

PubMed1977

Acute decrease of blood thyroid hormone by isovolemic exchange transfusion as a stimulus for pulse TSH release and its modifications by CNS Lesions.

The level of thyroid hormone in blood has been acutely decreased by about 20--30% within 20 min with the aid of isovolemic exchange transfusion (IET) of thyroid hormone free blood cell suspension (THFBCS) in three groups of rats: (1) intact control (C); (2) median eminence (ME)-lesioned; (3) thalamus (TH)-lesioned. The levels of thyroxine (T4) and TSH were measured by specific radioimmunoassay (RIA) before the transfusion and for 180 min after that. The level of T4 increased to the initial value at about 120 min after IET in C and ME-lesioned rats, while in TH it remained decreased until 180 min. Furthermore, at the end of IET the level of TSH in C and ME-lesioned rats was about 2--3 time higher than the initial value and its continuous decrease was observed until 180 min. In contrast, in TH-lesioned rats the increase of TSH level was delayed, being significant at 60 min only. It was concluded that IET of THFBCS acts as a stimulus of acute TSH release which was remarkably inhibited in TH-lesioned animals. In addition, the destruction of most of the ME did not apparently influence this response, as shown by essentially similar data obtained in C and ME-lesioned rats.

Animals↗

PubMed1977

Rapid disappearance of loading doses of thyroxine from blood and their excretion by the bile in rats.

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.

Animals↗

PubMed1977

Comparison of preventive effect of T3 and T4 on thyroxine release from thyroid induced by endogeneous TSH after TRH injection.

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.

Animals↗

PubMed1976

Acute redistribution of thyroxine after the administration of univalent anions, salicylate, theophylline and barbiturates in rats.

Rats were injected with [125I]L-thyroxine (T4) ip 16 h before the experiment and samples of blood were frequently taken from polyethylene tubing inserted into the femoral artery in anaesthetized and heparin injected animals, isovolaemia being maintained. In each sample of plasma T4 counts per ml were estimated with the aid of paper chromatography. Rapid decrease of circulating T4 level was found at 20 min after iv injection of various compounds (thiocyanate, iodide, fluoroborate, theophylline and salicylate) and a dose-response relationship was established between such a decrease and the administered dose of salicylate (5-160 mg/400 g b.w.). A similar decrease was observed at 60 min after ip injection of some general anaesthetics (thio-, pento- and allo-barbiturate, urethane) or tranquilizers (Innovar-Vet). Finally, an incrase of T4 fractional disposal rate was found between 120 and 480 min after the administration of some of the above mentioned anaesthetics and this effect was abolished by the administration of thiocyanate. It was concluded that there are two different effects of drugs on the circulating T4 level: 1. the immediate effect resulting apparently from a decreased plasma protein binding; 2. the prolonged effect which presumably results from the increased turnover of T4 by peripheral tissues, the metabolic basis of which remains unexplained.

Animals↗

PubMed1976

Altered response of blood thyroxine level after its acute depletion by isovolemic exchange transfusion in rats with lesions in hypothalamus and thalamus.

Bilateral electrolytic lesions were made in various areas of hypothalamus or thalamus on the 6th day of a period of daily radioiodide injections (1 or 5 muCi125I-daily per animal) in male rats weighing about 350 g. Such injections were continued for another 4 days and after 2 days of intermission the blood thyroid hormone was acutely depleted by isovolemic exchange transfusion of thyroid hormone free blood cell suspension. Relative changes of plasma thyroxine level were measured with the aid of paper chromatography in small aliquots of plasma frequently taken from the animals under maintaining isovolemia by replacing the removed plasma. It was found that in animals with various bilateral electrolytic lesions in hypothalamus (suprachiasmatic and paraventricular areas) the response of blood thyroxine level after the transfusion is similar as in sham-operated controls bearing unilateral subcortical lesion or in normal animals observed previously. On the other hand, the response in animals with thalamic lesions was repeatedly found to resemble that observed previously in thyroidectomized animals. Since the response of blood thyroxine level presumably results from changes of pituitary thyrotropic activity, it is concluded that in rats with thalamic lesions the normal response of hypothalamo-pituitary-thyroid axis was prevented. The mechanism of this action, however, remains to be elucidated.

Animals↗

PubMed1976

TRH induced thyroxine release from thyroid: its prevention by thyroxine influenced by actinomycin D and cycloheximide.

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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