Biomedical subjects

P Venditti

Publications and source records attributed to P Venditti.

At least 37 records · Page 2Linked to original sources

PubMed1999

Two-step synergism between the progesterone receptor and the DNA-binding domain of nuclear factor 1 on MMTV minichromosomes.

In contrast to its behavior as naked DNA, the MMTV promoter assembled in minichromosomes can be activated synergistically by the progesterone receptor and NF1 in a process involving ATP-dependent chromatin remodeling. The DNA-binding domain of NF1 is required and sufficient for stable occupancy of all receptor-binding sites and for functional synergism. Activation of purified minichromosomes is observed in the absence of SWI/SNF and can be enhanced by recombinant ISWI. Receptor binding to minichromosomes recruits ISWI and NURF38, but not brahma. We propose a two-step synergism in which the receptor triggers a chromatin remodeling event that facilitates access of NF1, which in turn stabilizes an open nucleosomal conformation required for efficient binding of further receptor molecules and full transactivation.

Adenosine Triphosphatases↗

PubMed1999

Protection against ischemia-reperfusion induced oxidative stress by vitamin E treatment.

The rat heart protection offered by vitamin E against oxidative stress after ischaemia-reperfusion was studied by using a new methodological approach. Functional recovery of hearts from ischaemia-reperfusion was correlated with a traditional index of oxidative stress such as lipid peroxidation and with antioxidant capacity and susceptibility to oxidants of the tissue evaluated by enhanced chemiluminescence techniques. Rats were treated with ten daily i.m. injections of 100 mg/kg body weight of vitamin E. The functional recovery during reperfusion (20 min, following 45 min ischaemia) of Langendorff preparations from control (vehicle-injected) and vitamin E treated rats was evaluated in terms of heart rate, left ventricular developed pressure (LVDP), double product (= heart rate. LVDP) and coronary flow recovery. Vitamin E treatment significantly improved functional recovery of heart rate, LVDP, double product and coronary flow. It also increased the level of vitamin E and reduced the levels of both malondialdehyde and hydroperoxides in the heart tissue at the end of the ischaemia-reperfusion protocol. In contrast, it did not affect the antioxidant capacity and the response of heart homogenates to in vitro oxidative stress measured after ischaemia-reperfusion. These results show a protective action of vitamin E treatment against lipid peroxidation and cardiac dysfunction associated with ischaemia-reperfusion. Although the precise mechanism of this protection is not evident, our model in part suggests a role of vitamin E other than as a free radical scavenger.

Animals↗

PubMed1999

Antioxidant-sensitive triiodothyronine effects on characteristics of rat liver mitochondrial population.

Whole mitochondrial population and three mitochondrial fractions were resolved by differential centrifugation from liver homogenates from euthyroid, hyperthyroid (ten daily i.p. injections of triiodothyronine (T3), 10 microg/100 g body weight) and hyperthyroid vitamin E-treated (ten daily i.m. vitamin E injections, 20 mg/100 g body weight) rats. Homogenates and mitochondrial preparations were examined for their protein content, oxidative capacity, lipid peroxidation, antioxidant status, and susceptibility to oxidative stress. In all groups, antioxidant level was smaller and oxidative capacity, lipid peroxidation, and susceptibility to oxidants were greater in the heavy mitochondrial fraction. T3 treatment was associated with increased oxidative capacity, lipid peroxidation, and susceptibility to oxidative stress, and decreased antioxidant levels in all preparations. It was also associated with increased mitochondrial protein content of homogenate and altered quantitative presence of the mitochondrial fractions. The vitamin E effects on the T3-induced changes were different for the different parameters. Vitamin E did not modify the mitochondrial protein content in liver and oxidative capacity of the various preparations, reduced the changes in both susceptibility to oxidants and contribution of each fraction to the whole mitochondrial population, and reinstated euthyroid values for antioxidant capacity and lipid peroxidation. The incomplete recovery of euthyroid resistance to oxidants in vitamin E-treated rats is due to the vitamin inability to reinstate the levels of both antioxidants and hemoproteins, on which such a resistance depends. The vitamin E effect on the composition of the mitochondrial population is more difficult to explain, because of the complexity of the mechanisms underlying the mitochondrial population modulation by thyroid hormone. However, available data suggest that such a modulation occurs through changes in the turnover of the mitochondrial fractions to which an induction of mitochondrial protein synthesis and accelerated antioxidant-sensitive degradation contribute in different measure.

Animals↗

PubMed1998

Assembly of MMTV promoter minichromosomes with positioned nucleosomes precludes NF1 access but not restriction enzyme cleavage.

To generate long arrays of nucleosomes within a topologically defined chromatin domain we have assembled minichromosomes on negatively supercoiled plasmid DNA with extracts from Drosophila preblastoderm embryos. These minichromosomes are dynamic substrates for energy-dependent nucleosome remodeling machines that facilitate the binding of various transcription factors but do not exhibit nucleosome positioning. In contrast, if such minichromosomes include the mouse mammary tumour virus (MMTV) promoter we find it wrapped around a nucleosome with similar translational and rotational position as in vivo . This structure precluded binding of NF1 to its cognate site at -75/-65 at salt concentrations between 60 and 120 mM, even in the presence of ATP, which rendered the NF1 site accessible to the restriction enzyme Hin fI. However, insertion of 30 bp just upstream of the NF1 site, which moves the site to the linker DNA, allowed ATP-dependent binding of NF1 to a fraction of the minichromosomes, even in the presence ofstoichiometric amounts of histone H1. The minichromosomes assembled in the Drosophila embryo extract reproduce important features of the native MMTV promoter chromatin and reveal differences in the ability of transcription factors and restriction enzymes to access their binding sites in positioned nucleosomes.

Adenosine Triphosphate↗

PubMed1998

Antioxidant-sensitive shortening of ventricular action potential in hyperthyroid rats is independent of lipid peroxidation.

The effects of substances able to reduce peroxidative processes on thyroid hormone-induced electrophysiological changes in ventricular muscle fibres were examined. For this study, 60 day old euthyroid and hyperthyroid rats were used. One group of hyperthyroid rats was untreated and the others were treated with vitamin E, N-acetylcysteine, and cholesterol, respectively. Hyperthyroidism was elicited by 10 day treatment with daily i.p. injections of triiodothyronine (10 microg/100 g body weight). Vitamin E and N-acetylcysteine were administered for 10 days by daily i.m. injections (20 mg/100 g body weight) and daily i.p. injections (100 mg/100 g body weight), respectively. Cholesterol was administered by cholesterol-supplemented diet (4%) from day 30. Hyperthyroidism induced a decrease in the whole antioxidant capacity and an increase in both lipid peroxidation and susceptibility to oxidative stress. Vitamin E and N-acetylcysteine administration to hyperthyroid rats led to reduction in lipid peroxidation and susceptibility to oxidative stress and to increase in antioxidant level, while the diet addition of cholesterol decreased lipid peroxidation but did not modify the other parameters. The hyperthyroid state was also associated with a decrease in the duration of the ventricular action potential recorded in vitro. The vitamin E and N-acetylcysteine administration attenuated the thyroid hormone-induced changes in action potential duration, which was however, significantly different from that of the euthyroid rats. In contrast, cholesterol supplementation did not modify the electrical activity of hyperthyroid heart. These results demonstrate that the triiodothyronine effects on ventricular electrophysiological properties are mediated, at least in part, through a membrane modification involving a free radical mechanism. Moreover, they indicate that the antioxidant-sensitive shortening of action potential duration induced by thyroid hormone is likely independent of enhanced peroxidative processes in sarcolemmal membrane.

Acetylcysteine↗

PubMed1998

Free radical involvement in doxorubicin-induced electrophysiological alterations in rat papillary muscle fibres.

OBJECTIVE: This work was designed to determine whether the doxorubicin-induced changes in heart electrical activity are due to increased free radical production and membrane oxidative damage. METHODS: Four groups of rats (60 days old) were used. One group was untreated and the others were treated with doxorubicin (DXR), DXR and vitamin E, and DXR and N-acetylcysteine (NAC), respectively. DXR was administered by single i.p. injection (20 mg/kg b.wt.). Vitamin E was administered by ten daily i.m. injections (100 mg/kg), while NAC (100 mg/kg) was injected i.p. 1 h before and 7 h after DXR. The effectiveness of the drug in inducing oxidative stress in different tissues and of the antioxidants in offering protection was established by determining antioxidant capacity, susceptibility to oxidative stress, and lipid peroxidation in heart, liver, and blood. The drug effect on heart electrical activity was determined by measuring the heart rate in vivo and action potential configuration in papillary muscle fibres in vitro. Heart lipid peroxidation and electrical activity were also examined in both vitamin E and NAC-treated rats. RESULTS: DXR treatment decreased antioxidant capacity and increased lipid peroxidation and susceptibility to oxidative stress in heart and blood, but not in liver. DXR administration to rats treated with antioxidants did not produce significant changes in antioxidant capacity and susceptibility to oxidative stress even in heart and blood. Furthermore, lipid peroxidation in heart and liver from DXR- and vitamin E-treated rats, and in liver from DXR- and NAC-treated rats was lower than in untreated controls. DXR treatment also increased the duration of ventricular action potentials in untreated rats, but not in antioxidant-treated rats. The treatment of control animals with the antioxidants affected lipid peroxidation, but not cardiac electrical activity. CONCLUSIONS: The protection offered by antioxidants against electrophysiological alterations indicates a free radical involvement in such alterations. In contrast, although electrical modifications are associated with increased peroxidative processes and both are prevented by the antioxidants, it is not yet clear whether a causative relationship exists between them.

Acetylcysteine↗

PubMed1998

Effect of phenobarbital treatment on characteristics determining susceptibility to oxidants of homogenates, mitochondria and microsomes from rat liver.

This study was designed to investigate the possible oxidative changes associated with alterations in cytochrome P450 levels in rat liver. Accordingly, extent of peroxidative processes, cytochrome and antioxidant content, capacity to face an oxidative stress were determined in liver microsomes, mitochondria, and homogenates from normal and phenobarbital (PB)-treated rats. Liver content of microsomal and mitochondrial proteins was also determined by the values of the activities of marker enzymes (glucose-6-phosphatase and cytochrome oxidase, respectively) in liver homogenate and in two cellular fractions. The increase in the liver content of microsomal and mitochondrial proteins indicated that PB caused proliferation of both smooth endoplasmic reticulum and mitochondrial population. Treatment with PB also gave rise to a general increase in peroxidative reactions (evaluated measuring malondialdehyde and hydroperoxides (HPs)), in the different cell compartments, even though HPs were not found significantly increased in mitochondrial fraction. The increase in peroxidative processes was associated with significant decreases in antioxidant concentration (expressed in terms of equivalent concentration of an antioxidant, such as the desferrioxamine), in all preparations from PB-treated rats. The response to oxidative stress in vitro (evaluated determining the parameters characterizing light emission from preparations stressed with sodium perborate) showed a substantial PB-induced increase in the susceptibility to oxidative challenge only in liver homogenate. The lack of changes in the mitochondrial preparations is likely due to decrease in concentration of both free radical producing species and antioxidants. The lack of changes in microsomal fraction is apparently in contrast with its lower oxidant capacity and higher content of cytochromes which are able to determine sensitivity to pro-oxidants. However, it could be due to the ability of cytochrome P450 to interact with the active oxygen species formed at its active center.

Animals↗

PubMed1997

Effect of training on antioxidant capacity, tissue damage, and endurance of adult male rats.

We studied the effects of physical training on antioxidant defences and susceptibility to damage induced by exhaustive exercise in tissues of adult (12 mo) rats. Therefore, untrained animals were sacrificed either at rest (n = 8) or immediately after swimming to exhaustion (n = 8). Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest (n = 8) or after exhaustive swimming (n = 8). Integrity of mitochondria and sarcoplasmic (SR) or endoplasmic (ER) reticulum of liver, heart, and muscle was assessed by measuring mitochondrial respiratory control and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on tissue antioxidant systems was examined by determining the glutathione peroxidase (GPX) and glutathione reductase (GR) activity and the overall antioxidant capacity (CA). Membrane integrity was unaffected by training in liver and muscle, and improved in heart of at rest animals, whereas lipid peroxidation was reduced in both liver and heart. Glutathione peroxidase and glutathione reductase activity, and overall antioxidant capacity were increased (p < 0.05) by training in liver and muscle. In heart, antioxidant capacity was increased from 0.21+/-0.01 to 0.33+/-0.02 (p<0.05), but glutathione peroxidase activity remained unchanged (p>0.05), and glutathione reductase activity was decreased from 3.56+/-0.08 to 2.27+/-0.10 micromol x min(-1) x g(-1) (p < 0.05). The exhaustive exercise gave rise to tissue damage irrespective of trained state, as documented by similar loss of SR and ER integrity, and increase (p<0.05) in lipid peroxidation found in exhausted trained and untrained rats. However, the above changes were elicited by exercise of greater duration in trained than in untrained rats (340+/-17 min and 233+/-6 min, respectively). These findings support the view that free radical-induced damage in muscle could be one of the factors involved in muscle fatigue. If so, the increased endurance in trained rats should reflect lengthening of the time required for the oxidative processes to sufficiently impair cell functions so as to make further exercise impossible.

Alkaline Phosphatase↗

PubMed1997

Effect of iodothyronines on electrophysiological properties of rat papillary muscle fibres.

We studied the effect of in vivo administration of 3,3',5-triiodo-L-thyronine (L-T3) and other iodothyronines to thyroidectomized rats on the heart rate and electrophysiological properties, recorded in vitro, from papillary muscle fibres. The treatment with a daily substitutive L-T3 dose (3.7 nmoles/100 g body weight) for ten days was associated with a significant increase of heart rate and reduction of the action potential duration (APD) in comparison to that recorded from thyroidectomized rats. Analogous changes were obtained by treatment with equimolar dose of iodothyronines, such as 3,3',5-triiodo-D-thyronine (D-T3), 3,3',5,5'-L-tetraiodothyronine (L-T4), and 3'-isopropyl-3,5-diiodothyronine (3'-Ip-T2), but not by treatment with 3,3',5'-L-triiodothyronine (L-rT3). Unlike the heart rate, APD was found in close correlation with the relative occupancy by iodothyronines of the heart thyroid hormone-specific nuclear sites reported in literature. Such a pattern was little modified when the stimulation rate of the preparations was increased from 1 Hz to 5 Hz, nearing the physiological rates. In fact, there were no significant APD changes for all groups, and only the significance of the APD difference between the T + L-T3 and T + L-rT3 groups was modified. In accordance to the expectations, L-T4 showed appreciable effects on APD at both frequencies tested, despite its small affinity for nuclear receptors. Indeed, it is well-known that a substantial proportion of the T4 effect derives from peripheral conversion to T3. Therefore, our results support the hypothesis that the long-term effects of thyroid hormone on ventricular electrophysiological properties are induced via synthesis of proteins that are part of ionic channels, through a pathway involving hormone interaction with the cell nucleus.

Action Potentials↗

PubMed1997

Action potential configuration in heart papillary muscles from female rats in different thyroid states.

We have studied the effects of thyroidectomy and the in vivo administration of different triiodothyronine (T3) doses in thyroidectomized female rats on electrophysiological properties, measured in vitro, of the anterior and posterior papillary muscle fibers from the right ventricle. In each thyroid state, the action potential duration (APD) measured by stimulating at 1 Hz was shorter for the posterior papillary muscle. APD from both preparations was found significantly lengthened in thyroidectomized animals in comparison to euthyroid controls. APD was shortened owing to treatment of thyroidectomized rats with T3 doses up to 10 micrograms/100 g body weight every second day. Treatment with larger doses of T3 tended to restore the values of APD found for ventricular fibres from both controls and thyroidectomized animals treated with substitutive T3 doses (5 micrograms/100 g body weight every second day). As the stimulation rate was increased from 1 to 5 Hz, APD increased in both preparations of all groups. The changes were of different amounts but the APD difference between the rat groups, which were significant at 1 Hz, remained significant at 5 Hz, while the differences between anterior and posterior preparations were cancelled in animals treated with 50 micrograms of T3 and reversed in those treated with 100 micrograms.

Action Potentials↗

PubMed1997

Modifications of antioxidant capacity and heart electrical activity induced by hydroperoxide in normal and vitamin E-fed rats.

Wistar rats, fed control or vitamin E-supplemented diet, were subjected to oxidative stress by a ten day treatment with daily intraperitoneal dose of tert-butyl hydroperoxide (TBHP) (0.1 mumol/100 g body weight). The effectiveness of both diet and hydroperoxide treatment was established by determining the antioxidant capacity of blood, liver, and heart with an enhanced luminescence method. While the diet addition of vitamin E increased the antioxidant capacity of all the tissues in treated and untreated animals, the hydroperoxide treatment failed to decrease liver antioxidant capacity in control diet fed animals. The effect of the reiterated production of free radicals on electrophysiological properties of myocardium was determined by studying the heart rate in vivo and the time course of the surface electrical activity in papillary muscle fibers in vitro. In vivo, a significant tachycardia was found only in TBHP-treated, normal diet fed rats. The duration of action potential, recorded in Krebs' solution at 26 degrees C, was not affected by diet in untreated animals but was modified by hydroperoxide treatment in a diet-dependent way: shortened in normal diet-fed rats and lengthened in vitamin E-supplemented diet-fed rats. On the basis of analogies with the results of electrophysiological recordings on different preparations subjected to oxidative stress in vitro, we suggest that the changes of action potential duration might depend on relative levels of added pro-oxidant and cell antioxidants.

Action Potentials↗

PubMed1997

Vitamin E administration attenuates the tri-iodothyronine-induced modification of heart electrical activity in the rat.

This work was designed to determine whether the thyroid-hormone-induced modifications of heart electrical activity are, at least in part, due to increased free radical production. For this study, 60-day-old euthyroid, hyperthyroid and hyperthyroid vitamin-E-treated rats were used. Hyperthyroidism, elicited by a 10 day treatment with tri-iodothyronine, induced an increase in lipid peroxidation without changing the level of antioxidants. Intraperitoneal vitamin administration to hyperthyroid rats led to a reduction in lipid peroxidation and a non-significant increase in antioxidant level. The hyperthyroid state was also associated with an increase in heart rate measured in vivo and a decrease in the duration of the ventricular action potential recorded in vitro. Administration of vitamin E attenuated the thyroid-hormone-induced changes in heart rate and action potential duration, which were, however, significantly different from those of the control euthyroid rats. These results suggest that vitamin E protects hyperthyroid heart against lipid peroxidation by mechanisms that may be independent of the changes in antioxidant systems. Moreover, the reduction in the tri-iodothyronine effects on heart electrophysiological properties indicates that such effects are mediated, at least in part, through a membrane modification, probably related to increased lipid peroxidation, involving a free radical mechanism.

Action Potentials↗

PubMed1997

Effect of thyroid state on lipid peroxidation, antioxidant defences, and susceptibility to oxidative stress in rat tissues.

The effects of altered thyroid states on lipid peroxidation, antioxidant capacity, and susceptibility to oxidative stress of rat tissues were examined. Hypothyroidism was induced by administering methimazole in drinking water for 15 days. Hyperthyroidism was elicited by a 10-day treatment of hypothyroid rats with tri-iodothyronine (10 micrograms/100 g body weight). In tissues of hypothyroid rats the lipid peroxidation was not modified, whereas in hyperthyroid rats lipid peroxidation increased in liver and heart but not in skeletal muscle. The glutathione peroxidase activity increased significantly in heart and muscle of hypothyroid rats and in muscle of hyperthyroid rats. The glutathione reductase activity was not modified in tissues of hypothyroid and hyperthyroid rats. In both rat groups the whole antioxidant capacity of tissues decreased, but significantly only in liver and heart. The results obtained studying the response to oxidative stress in vitro indicated that the susceptibility to oxidative challenge was increased in all tissues of hyperthyroid rats and in heart and muscle of hypothyroid animals. These results are explainable in terms of tissue variations in haemoprotein content and/or of antioxidant capacity. Since it has been reported that hypothyroidism offers in vivo protection against free radical damage, we suggest that such an effect could be due to greater effectiveness of cellular defence systems different from antioxidant ones.

Analysis of Variance↗

PubMed1996

Tissue protection against oxidative stress.

We used an enhanced luminescence technique to study the response of rat tissues, such as liver, heart, muscle and blood, to oxidative stress and to determine their antioxidant capacity. As previously found for liver homogenate, the intensity of light emission (E) of tissue homogenates and blood samples, stressed with sodium perborate, is dependent on concentration, and the dose-response curves can be described by the equation E = a.C/exp(b.C). The b value depends on the antioxidant defence capability of the tissues. In fact, it increases when homogenates are supplemented with an antioxidant, and is correlated with tissue antioxidant capacity, evaluated by two previously set up methods both using the same luminescence technique. Our results indicate that the order of antioxidant capacity of the tissues is liver > blood > heart > muscle. The a value depends on the systems catalysing the production of radical species. In fact, it is related to the tissue level of hemoproteins, which are known to act as catalysts in radical production from hydroperoxides. The equation proposed to describe the dose-response relation is simple to handle and permits an immediate connection with the two characteristics of the systems analysed which determine their response to the pro-oxidant treatment. However, the equation which best describes the above relation for all the tissues is the following: E = alpha. C/exp(beta.C delta). The parameter delta assumes values smaller than 1, which seem to depend on relative amounts of tissue hemoproteins and antioxidants. The extension of the analysis to mitochondria shows that they respond to oxidative stress in a way analogous to the tissues, and that the adherence of the dose-response curve to the course predicted from the equation E = a.C/exp(b.C) is again dependent on hemoprotein content.

Animals↗

PubMed1996

Antioxidants, tissue damage, and endurance in trained and untrained young male rats.

It is well known that physical training permits an animal to respond successfully to exercise loads of various types, intensities, and durations. Furthermore, the trained animal can sustain the activity for a long period before the fatigue becomes limiting. The effects of physical training on the antioxidant defenses of tissues and on their susceptibility to damage induced by exhaustive exercise have been investigated. Therefore, untrained rats were sacrificed either at rest or immediately after swimming to exhaustion. Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest or after exhaustive swimming. Homogenates of liver, heart, and muscle were used for biochemical determinations. Mitochondrial and sarcoplasmic (SR) or endoplasmic (ER) reticulum integrity was assessed with measurements of respiratory control index and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on the antioxidant protection systems of tissues was examined by determining the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity. Mitochondrial, SR, and ER integrity and lipid peroxidation were similar in trained and untrained at rest animals, whereas the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity of tissues were greater in trained animals. The exhaustive exercise gave rise to tissue damage irrespective of the trained state, as documented by similar loss of SR and ER integrity, and by increase in lipid peroxidation found in exhausted trained and untrained rats. Because exercise endurance capacity was greatly increased by training, our results suggest that free radical-induced damage in muscle could be one of the factors terminating muscle effort. In effect, the greater antioxidant level should allow trained muscle to withstand oxidative processes more effectively, thus lengthening the time required so that the cell function is sufficiently damaged as to make further exercise impossible.

Animals↗

PubMed1996

Effect of cold exposure on electrophysiological properties of rat heart.

Male rats exposed to the cold (4 degrees C) for five or ten days exhibited modifications in their thyroid state, as documented by increases in serum thyroid hormone levels, to which differently graded modifications of heart weight/body weight ratio, heart rate, and resting metabolic rate were associated. The values of the above mentioned thyroid state indicators returned to those of the control when the animals, kept at cold for ten days, were re-exposed to room temperature (24 degrees C) for an additional 10 days. The configuration of action potentials, recorded in vitro at 26 degrees C from fibres of anterior papillary muscles, was different in control rats of different age and was affected by prolonged cold exposure. In fact, the action potential duration (APD) increased after ten days of cold exposure. In the re-exposed group the APD was not different from that of the controls. Such a pattern was not significantly modified when the stimulation frequency increased from 1 Hz to 5 Hz. The above results suggest that in cold exposure, as in experimental hyperthyroidism, thyroid hormone might exert a cardiac chronotropic effect by modifying heart electrophysiological properties. Thus thyroid hormone should play a basic role during the exposure to cold environment, stimulating the body metabolism and increasing heart rate as a response to the requirement for greater tissue perfusion.

Action Potentials↗

PubMed1996

Effect of T3 administration on electrophysiological properties of lizard ventricular muscle fibres.

We investigated the effects on the electrophysiological properties of ventricular muscle fibres from lizards kept at 20 degrees C of mild and severe hyperthyroidism. The hyperthyroidism was induced by a 4-day treatment with either 0.025 or 1.0 microgram triiodothyronine g-1 body weight, documented by increased serum levels of thyroid hormone. Triiodothyronine treatment did not modify the duration of the action potential recorded in vitro at 25 degrees C from ventricular muscles stimulated at 1 Hz. Recordings at higher temperatures were associated with a faster repolarization phase and a decrease of of action potential duration in both euthyroid and hyperthyroid animals. However, in lizards treated with 1.0 microgram triiodothyronine . g-1 body weight, the 90% repolarization recovery times at 30 and 35 degrees C (95.6 +/- 14.9 ms and 53.0 +/- 6.0 ms, respectively), were significantly shorter than normal (177.6 +/- 29.2 and 107.2 +/ 18.1 ms, respectively). Action potential duration was also dependent on stimulation frequency of the preparations. Increased frequency led to significant decrease of the duration of action potentials recorded at 25 degrees C. In euthyroid preparations the reductions in 90% repolarization recovery time, owing to increase in stimulation frequency to 2.5 and 5 Hz, were 19.3 +/- 1.7 and 35.6 +/- 2.0 ms, respectively. In hyperthyroid preparations, the reductions in the 90% recovery time due to stimulus frequency increases varied from 35.4 +/- 1.9 and 58.1 +/- 2.1 ms at low hormone doses to 38.9 +/- 2.0 and 58.2 +/- 2.1 ms at high hormone doses. As a result of these differences, the action potential durations recorded from the two hyperthyroid preparations at high stimulation rates were shorter than from euthyroid preparations. The results obtained suggest that lizard cardiac tissue is responsive to hormone action at low environmental temperature, but the effects of such action become evident when the temperature and heart rate increase.

Action Potentials↗

PubMed1996

Effect of exercise on tissue anti-oxidant capacity and heart electrical properties in male and female rats.

We studied the changes in the anti-oxidant capacity of tissues, such as heart, liver, and blood in male and female rats, as a parameter for evaluating oxidative stress after either a prolonged (210 min) or an exhausting bout of swimming. Furthermore, we also investigated exercise-induced changes in the electrophysiological properties, measured in vitro, of papillary muscle fibres. Small decreases of anti-oxidant capacities after prolonged exercise [0.10 (SEM 0.04) in heart, 0.43 (SEM 0.19) in liver, 0.22 (SEM 0.05) in blood] and greater decreases after exhausting exercise [0.23 (SEM 0.04) in blood] were found in tissues from the male rats. For the female rats, similar changes were found only in the blood [0.11 (SEM 0.07) and 0.35 (SEM 0.06) for prolonged and exhausting exercise respectively]. Liver and heart anti-oxidant capacity remained unchanged after prolonged exercise, while after exhausting swimming it underwent a decrease almost the same as found in the male rats, though the swimming time to exhaustion (endurance capacity) was much greater [706 (SEM 10) min and 444 (SEM 32) min for the females and males, respectively]. The duration of the action potential, recorded from papillary muscle fibres, underwent changes related to the decreases in heart anti-oxidant capacity. In fact, the action potential duration (APD) was shorter only in preparations from the male rats after prolonged exercise, but in all preparations after exhausting exercise. After such exercise, the APD was similar for the male and female rats [37.1 (SEM 3.4) ms and 37.0 (SEM 3.6) ms, respectively]. Such a pattern was independent of stimulation frequency, since it was found substantially unchanged when the frequency was increased from 1 to 5 Hz. We concluded that the different susceptibilities to the effects of physical exercise, exhibited by tissues from these male and female rats might have been related to different capacities to oppose oxidative stress effectively.

Action Potentials↗