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S Di Meo

Publications and source records attributed to S Di Meo.

50 records · Page 3Linked to original sources
PubMed1991

Thyroid state and electrical properties of rat papillary muscle fibres.

We have studied the effects of in vivo alterations of thyroid state on the electrophysiological properties, measured in vitro, of rat papillary muscle fibres. The duration of the action potential, recorded from single cells of papillary muscle obtained from 60 day old rats, thyroidectomized at weaning, was larger than in preparations of euthyroid animals of same age. The treatment of thyroidectomized rats with T3 physiological doses restored the values of action potential duration present in euthyroid animals of same age. The data dealing with the time course of these variations indicate a late effect of thyroidectomy or T3 treatment. The hyperthyroid state, obtained by treatment of thyroidectomized rats with larger doses of T3, was associated with a significant reduction in the action potential. Action potential duration is frequency dependent. As the stimulation rate was increased from 1 to 5 Hz, this duration increased in all groups. However the difference found among the rat groups remained significant. Propranolol had virtually no effect on action potentials from fibres of euthyroid animals and those in altered thyroid state.

Action Potentials↗
PubMed1989

Modulation of the heart rate by thyroid hormone in the newborn rat.

Confirming the literature data the authors describe that the heart rate is smaller in the newborn rats than in adult ones and increases until the adult values during the first two weeks of life. On the other hand, the blood thyroid hormone exhibits the same pattern, showing an early postnatal increment. As, according the Adolph's data (1967), the heart rate enhancement is not due to the catecholamines, the authors suppose that such enhancement might conceivably depend on thyroid hormone increment.

Age Factors↗
PubMed1989

The direct effect of the thyroid hormone on cardiac chronotropism.

To establish whether thyroid hormone modifies the heart rate directly or through an action on other neuroendocrine modulators, the authors have examined several animals models differing in the plasma levels of such compounds. Induction of the hypothyroid state in rats produced a slow onset of bradycardia, which may be removed by a prolonged triiodothyronine treatment. The involvement of TSH was excluded as, by comparing thyroidectomized, hypophysectomized and cold exposed rats, the heart rate was found to vary according to the thyroid levels and not to the TSH levels. Moreover growth hormone, corticotropin and gonadotropins do not influence the heart rate, as the bradycardia induced by hypophysectomy was fully removed by triiodothyronine treatment. The lack of influence by ACTH and GnH was confirmed by treatment of thyroidectomized rats with corticosteroids or testosterone, respectively. Finally, thyroid hormone did not act on the heart rate by changing the norepinephrine output at the sympathetic nerve endings in the heart. In fact, thyroidectomy produced a more intense bradycardia than sympathectomy, and such bradycardia was equally removed by triiodothyronine treatment in thyroidectomized rats and in thyroidectomized and then sympathectomized ones. The authors suggest that the direct effect of the thyroid hormone on cardiac chronotropism is due to an early enhancement of beta-adrenoceptors, followed by a late modification of the electrophysiological properties of the myocardium.

Animals↗
PubMed1988

Thyroid hormone and the mitochondrial population in the rat heart.

The effects of the thyroid hormone on the number and protein content of mitochondria were investigated in rat heart. The specific mitochondrial population, determined by direct counting, was estimated to be about 3.7 X 10(11) mitochondria per g wet weight in young hypothyroid male rats (T) and about 2.4 X 10(11) (65%) in euthyroid animals, sex- and age-matched. Triiodothyronine (T3) treatment of T animals restored the levels to normal values. The protein content per mitochondrion, on the contrary, was higher in euthyroid animals or hypothyroid animals, following T3 treatment, compared to T. Finally, thyroid hormone enhanced the heart mass and, therefore, the cardiocytal and mitochondrial populations of the whole organ. These results differ from previous data from our laboratory indicating that liver weight is increased by thyroid treatment, albeit at a slower rate, while the number of mitochondria per g tissue increases and the protein content per mitochondrion decreases. In conclusion, the effects of the thyroid hormone on mitochondria are different in the hepatocyte and in the cardiocyte. It appears that the hormone differently modulates the machinery of mitochondrial protein synthesis in the two target cells according to the physiological role of mitochondria in liver and heart cells, i.e. heat production or mechanical energy output, respectively.

Animals↗
PubMedDate not supplied

Thyroid state and mitochondrial population during maturation and ageing.

The authors have determined the serum thyroid hormone levels [total and free triiodothyronine (T3), thyroxine (T4)], the liver T3 content, the mitochondrial alpha-glycerophosphate dehydrogenase activity (alpha-GPDH) and the number of mitochondria per cell in the rat from birth to old age. The serum levels of both thyroid hormones are modified with maturation and ageing in an essentially similar way: they increase from low values at birth to remarkably high values around 12 days, and then remain constant. The T3 liver content firstly increases (from birth to 14 days of life) and then maintains constant values. During the first two postnatal weeks, therefore, free serum T3 and liver T3 display a similar behavior. The alpha-GPDH activity of liver mitochondria was found constant from birth to old age. This might suggest either that the control of the alpha-GPDH activity is, at birth, under complex hormonal control, or that the nuclear receptors associated with the alpha-GPDH genes are precociously synthesized. The number of mitochondria per cell, at birth, is half the adult values, strongly increasing in number at weaning and remaining constant afterwards. The effect of thyroid hormones on the mitochondrial population during maturation, when low levels of serum T3 and T4 occur naturally, appears to be quite different from that induced experimentally by thyroidectomy.

Aging↗
PubMedDate not supplied

Mitochondria in exercise-induced oxidative stress.

In recent years it has been suggested that reactive oxygen species (ROS) are involved in the damage to muscle and other tissues induced by acute exercise. Despite the small availability of direct evidence for ROS production during exercise, there is an abundance of literature providing indirect support that oxidative stress occurs during exercise. The electron transport associated with the mitochondrial respiratory chain is considered the major process leading to ROS production at rest and during exercise. It is widely assumed that during exercise the increased electron flow through the mitochondrial electron transport chain leads to an increased rate of ROS production. On the other hand, results obtained by in vitro experiments indicate that mitochondrial ROS production is lower in state 3 (ADP-stimulated) than in state 4 (basal) respiration. It is possible, however, that factors, such as temperature, that are modified in vivo during intense physical activity induce changes (uncoupling associated with loss of cytochrome oxidase activity) leading to increased ROS production. The mitochondrial respiratory chain could also be a potential source of ROS in tissues, such as liver, kidney and nonworking muscles, that during exercise undergo partial ischemia because of reduced blood supply. Sufficient oxygen is available to interact with the increasingly reduced respiratory chain and enhance the ROS generation. At the cessation of exercise, blood flow to hypoxic tissues resumes leading to their reoxygenation. This mimics the ischemia-reperfusion phenomenon, which is known to cause excessive production of free radicals. Apart from a theoretical rise in ROS, there is little evidence that exercise-induced oxidative stress is due to its increased mitochondrial generation. On the other hand, if mitochondrial production of ROS supplies a remarkable contribution to exercise-induced oxidative stress, mitochondria should be a primary target of oxidative damage. Unfortunately, there are controversial reports concerning the exercise effects on structural and functional characteristics of mitochondria. However, the isolation of mitochondrial fractions by differential centrifugation has shown that the amount of damaged mitochondria, recovered in the lightest fraction, is remarkably increased by long-lasting exercise.

Animals↗
PubMedDate not supplied

Modification of electrophysiological properties of rat heart with age.

The authors have determined the serum thyroid hormone levels [total (TT3) and free (FT3) triiodothyronine], the heart weight/body weight ratio and the heart rate of differently aged male rats. The variations of these parameters show a modification of thyroid state as a function of ageing. The authors have also recorded, at about 26 degrees C, resting and action potentials from single cells of papillary muscles isolated from the same groups of rats. The animals in the higher thyroid state exhibited a repolarization speed higher than the other animals. The thyroidectomy, performed on 50 day old rats, and T3 treatment of the thyroidectomized rats give rise to modifications of repolarization speed and then of action potential duration analogous to ones obtained in previous study for animals thyroidectomized at 30 days of age. These data demonstrate that the modifications of heart electrophysiological properties with age, are due fundamentally to thyroid state modifications. The results suggest also that the cardiac chronotropism modifications which the rat undergoes as a function of ageing are due to the changes of levels of thyroid hormone which might exert its effect by modifying the ion channel kinetics as well as the cardiac receptors.

Action Potentials↗
PubMedDate not supplied

Ventricular electrophysiological properties in normal and congenitally hypothyroid neonatal rats.

The serum thyroid hormone levels [total (TT3) and free (FT3) triiodothyronine] and the heart rates were determined in neonatal rats of different ages (1-5-10 days). Thyroid hormone levels increase gradually in the first 10 days of age. The heart rate, tested at a body temperature of 37 degrees C, also increases during the same period. As the increase in heart rate in this phase of rat life is not due to the catecholamines, it is suggested that such an increase might depend on the increased thyroid hormone activity. On the other hand in congenitally hypothyroid rats the levels of both hormones and heart rates are lower than in normal animals of the same age. The electrophysiological properties of ventricular muscle fibres include a longer action potential, irrespective of stimulation frequency, in younger, naturally hypothyroid animals. The duration of action potential is greater in the congenitally hypothyroid animals, at all ages. These data demonstrate that, as in young and adult rats, the age-related modifications in heart rate, found in neonatal rats, might be due to thyroid dependent modifications of cardiac electrophysiology.

Action Potentials↗
PubMedDate not supplied

Effect of thyroidectomy and in vivo administration of triiodothyronine on DNA synthesis in isolated mitochondria.

The experimental conditions were studied which allow hormonal levels to affect the incorporation of labelled deoxyribonucleosides triphosphates (dNTP's) into mitochondrial DNA by isolated liver mitochondria, obtained either from thyroidectomized young male rats (T) or from animals of the same age thyroidectomized and then treated with triiodothyronine (T + T3). It was demonstrated that: (a) extramitochondrial DNA, on which extramitochondrial DNA polymerase may act, was absent; (b) the permeability to dNTP's, the thymidine kinase activity, the energy supply, and the nuclease activities were unaffected by hormonal conditions; (c) the bacterial contaminations contribute for only 1% to incorporation. The characterization of incorporation product showed that: (a) such product was indeed DNA, as it was DNase-degradable for about 90%; (b) the labelled DNA was indeed mitochondrial DNA, as a 10 minutes preincubation with acriflavine or ethydium bromide (Eth. Br.) inhibited the synthesis by 90%.

Animals↗
PubMedDate not supplied

DNA synthesis in isolated mitochondria: effect of thyroidectomy and of triiodothyronine administration in vivo.

The incorporation was studied of labelled deoxy-ribonucleosides triphosphates into acid-insoluble material by isolated liver mitochondria, obtained from either normal young male rats, or thyroidectomized at weaning, or thyroidectomized and then treated with triiodothyronine (T3). The incorporation extents in normal animals decreased with the age starting from the weaning until the 210th day. Thyroidectomy reduced the incorporation extent to about 70% of the values observed in normal animals. During the T3 treatment of thyroidectomized rats a sharp increase of incorporation was observed one day after the first administration, followed by a decrease from the 1st to the 3rd day; successively the incorporation extent remained unchanged until the 12th day. Finally, evidence was provided that T3 doses used were thyreomimetic and definitely lower than the thyreotoxic ones.

Aging↗