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PubMed1992

Beta-adrenergic blockade for the treatment of hyperthyroidism.

PURPOSE: To review the clinical and biochemical effects of beta-adrenergic blocking drugs on hyperthyroidism. MATERIALS AND METHODS: Studies published since 1972 were identified through a computerized search of MEDLINE and extensive searching of the bibliographies of the articles identified. Based on an understanding of the differences in beta-blocker metabolism in euthyroid and hyperthyroid patients, we reviewed the differences in pharmacokinetics and metabolic and clinical outcomes during their use in hyperthyroidism, as reported in the articles reviewed. RESULTS: beta Blockers have been used to modify the severity of the hyperadrenergic symptoms of hyperthyroidism for the past 20 years. The clinical efficacy of these agents is affected by hyperthyroid-induced alterations in their gastrointestinal absorption, hepatic metabolism, and renal excretion. The mechanisms whereby these clinical changes are effected is unknown. The agents differ in their beta 1 cardioselectivity, membrane-stabilizing activity, intrinsic sympathomimetic activity, and lipid solubility. They do not appear to alter synthesis or secretion of thyroid hormone by the thyroid gland. Their effects on thyroxine metabolism are contradictory. Decreased thyroxine to triiodothyronine conversion is caused by some, but not all, beta blockers, and this appears to correlate with membrane-stabilizing activity. There does not appear to be any alteration in catecholamine sensitivity during beta-adrenergic blockade. CONCLUSIONS: The principal mechanism of action of beta blockers in hyperthyroidism is to antagonize beta-receptor-mediated effects of catecholamines. beta Blockers are effective in treating hypermetabolic symptoms in a variety of hyperthyroid states. Used alone, they offer significant symptomatic relief. They are also useful adjuvants to antithyroid medications, surgery, and radioactive iodide treatment in patients with Graves' disease and toxic nodular goiters.

Adrenergic beta-Antagonists↗

PubMed1990

Enhanced activity of the tricarboxylate carrier and modification of lipids in hepatic mitochondria from hyperthyroid rats.

The effect of hyperthyroidism on the activity of the mitochondrial tricarboxylate carrier has been studied. The activity of this transporting system in liver mitochondria was quantitatively determined by the rate of malate-[14C]citrate exchange using the 1,2,3-benzene-tricarboxylate inhibitor stop technique. It has been found that the rate of citrate uptake is significantly enhanced in liver mitochondria from hyperthyroid rats as compared to that obtained in mitochondria from control rats. Kinetic analysis of the malate-citrate exchange reaction indicates that only the Vmax of this transporting process is enhanced, while there is practically no change in the Km values. Inhibitor titrations with the inhibitor palmitoyl-CoA show that mitochondria from hyperthyroid rats require the same concentrations of inhibitor to produce 100% inhibition of citrate uptake as control mitochondria, suggesting that the amount of functional translocase enzyme present is unaffected. The Arrhenius plot characteristics differ for tricarboxylate carrier activity in mitochondria from hyperthyroid rats as compared with control rats in that the break point of the biphasic plot decreases from 18.1 +/- 1.4 degrees C in controls to 12.9 +/- 1.2 degrees C in hyperthyroid animals. The hepatic mitochondrial lipid composition is altered significantly in hyperthyroid rats; the total cholesterol decreases and the phospholipids increase. The liver mitochondrial phospholipid composition is altered significantly in hyperthyroid rats. In particular negatively charged phospholipid cardiolipin increases by more than 50%. Minor alterations were found in the pattern of fatty acids. The thyroid hormone induced change in the activity of the tricarboxylate carrier can be ascribed either to a general modification of membrane lipid composition which increases the membrane fluidity and in turn the mobility of the carrier or to a more localized change of lipid domain (cardiolipin content) surrounding the carrier molecule in the mitochondrial membrane.

Animals↗

PubMed1991

Relationships between fatty acid synthesis and lipid secretion in the isolated perfused rat liver: effects of hyperthyroidism, glucose and oleate.

Various studies on the effects of thyroid status on hepatic fatty acid synthesis have produced conflicting results. Several variables (e.g., plasma free fatty acid and glucose concentrations) are altered simultaneously by thyroid status and can affect fatty acid synthesis. To evaluate the effects of these variables, hepatic fatty acid synthesis (lipogenesis) was studied in isolated perfused livers from normal and triiodothyronine-treated rats. Livers were perfused with media containing either 5.5 or 25 mM glucose without fatty acid, or 5.5 mM glucose and 0.7 mM oleate. Rates of lipogenesis were determined by measurement of incorporation of 3H2O into fatty acids. Lipogenesis in livers from hyperthyroid animals exceeded that of controls, when perfused with 5.5 mM glucose with or without oleate. Perfusion with 25 mM glucose increased lipogenesis in both euthyroid and hyperthyroid groups to the same level, abolishing this difference between them. Perfusion with oleate reduced rates of lipogenesis by livers from euthyroid and hyperthyroid rats to a similar extent, but stimulated secretion of radioactive fatty acid in phospholipid and free fatty acid fractions. Oleate increased ketogenesis by livers from normal and triiodothyronine-treated rats, with higher rates of ketogenesis in the triiodothyronine-treated group. When oleate was omitted, ketogenesis in the presence of 5.5 mM glucose by the hyperthyroid group was similar to that of euthyroid controls, while ketogenesis was decreased in the hyperthyroid group relative to controls when perfused with 25 mM glucose. About 30% of the radioactivity incorporated into the total fatty acid of both groups was recovered in palmitate, with the remainder in longer chain saturated and unsaturated fatty acids. In both euthyroid and hyperthyroid groups, the ratio of triacylglycerol:phospholipid fatty acid radioactivity was not only less than predicted (based on synthetic rates of PL and TG) but also was decreased in perfusions with exogenous oleate compared to perfusions without oleate. In perfusions with oleate, both groups incorporated twice as much radioactivity into phospholipid as into triacylglycerol. The data suggest the following concepts: while hepatic fatty acid synthesis and oxidation are increased simultaneously in the hyperthyroid state, de novo synthesized fatty acids seem to be poorer substrates for oxidation than are exogenous fatty acids, and are preferentially incorporated into phospholipid, while exogenous fatty acids are better substrates for oxidation and esterification to triacylglycerol. The preferential utilization of de novo synthesized fatty acid for phospholipid synthesis may be an important physiologic adaptation insuring a constant source of fatty acid for membrane synthesis.

Animals↗

PubMed1986

Basal and glucose- and arginine-stimulated serum concentrations of insulin, C-peptide, and glucagon in hyperthyroid patients.

The effect of oral glucose and arginine infusion on plasma glucose, glucagon, serum insulin, and C-peptide concentrations was evaluated in 16 patients with hyperthyroid Graves' disease and in ten euthyroid age- and sex-matched normal subjects. Basal plasma glucose concentrations were significantly higher in the hyperthyroid patients, but the plasma glucose response following glucose and arginine administration was similar in the two groups. The insulin response was similar in the hyperthyroid and normal subjects after glucose administration and significantly lower during arginine infusion in the hyperthyroid patients. The serum C-peptide response to both glucose and arginine administration was markedly blunted in the hyperthyroid patients, and the plasma glucagon response to arginine infusion was decreased. These results suggest that pancreatic beta and alpha cell secretory function is impaired in hyperthyroidism as assessed by C-peptide and glucagon secretion following oral glucose administration and arginine infusion. The apparent discrepancy between C-peptide and insulin secretion in the hyperthyroid patients following glucose administration might be due to diminished hepatic extraction of insulin or enhanced metabolism of C-peptide.

Adult↗

PubMed1995

Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism.

Hyperthyroidism is associated with an impairment of growth hormone (GH) responses to secretagogues. The aim of this study was to evaluate the effect of acipimox, an antilipolytic agent able to decrease free fatty acids (FFA), on GH response to GH-releasing hormone (GHRH) in hyperthyroid and normal control subjects. We studied six men with hyperthyroidism; seven normal men served as control subjects. Each subject underwent treatment with (1) 2 tablets of placebo orally or (2) 500 mg acipimox orally, 120 minutes before intravenous (IV) injection of 1 microgram/kg GHRH-(1-29)NH2. GH response to GHRH in hyperthyroid patients was markedly reduced; the mean peak GH response (9.6 +/- 1.0 microgram/L) and the area under the GH response curve (12.9 +/- 1.3 micrograms/L x 2 h) were lower than those of control subjects (25.7 +/- 1.8 micrograms/L, P < .05; 28.7 +/- 2.1 micrograms/L x 2 h, P < .05). Hyperthyroid patients had higher baseline levels of plasma FFA than control subjects (998.0 +/- 38.9 v 498.0 +/- 36.0 muEq/L, P < .01). Acipimox decreased FFA levels in both hyperthyroid and control subjects; the lowest FFA levels of hyperthyroid subjects induced by acipimox were similar to those of control subjects. After acipimox pretreatment, GH responses to GHRH increased significantly (P < .05); the mean peak plasma GH level (25.9 +/- 4.6 micrograms/L) was similar to the peak GH levels of control subjects during the GHRH test, and the area under the GH response curve (41.1 +/- 6.7 micrograms/L x 2 h) was even higher than that of control subjects with the GHRH test.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1991

Pharmacokinetics of methimazole in normal cats and cats with hyperthyroidism.

The intravenous and oral disposition of the antithyroid drug methimazole was determined in 10 clinically normal cats and nine cats with naturally occurring hyperthyroidism. After intravenous administration of 5 mg methimazole, the mean residence time was significantly (P less than 0.05) shorter in the cats with hyperthyroidism than in the normal cats, but there was no significant difference between the mean values for total body clearance (CL), steady state volume of distribution (Vdss), terminal elimination rate constant (ke), or serum terminal half-life (t1/2) in the two groups of cats. After oral administration, the mean bioavailability of methimazole was high in both the normal cats (77.6 per cent) and cats with hyperthyroidism (79.5 per cent). The values for mean residence time, ke and serum terminal t1/2 after oral dosing were significantly shorter in the cats with hyperthyroidism than in the normal cats. However, after oral administration of methimazole there were no significant differences between the mean values for CL, Vdss, bioavailability and maximum serum concentrations or the time for maximal concentrations to be reached in the two groups of cats. Overall, most pharmacokinetic parameters for methimazole were not altered by the hyperthyroid state. However, the cats with hyperthyroidism did show a trend toward faster elimination of the drug compared with the normal cats, similar to what has been previously described for the antithyroid drug propylthiouracil in cats. These results also indicate that methimazole is well absorbed when administered orally and has a higher bioavailability than that of propylthiouracil in cats with hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1987

Lack of circulating thyroid stimulating immunoglobulins in cats with hyperthyroidism.

Although feline hyperthyroidism has become a commonly diagnosed disorder of older cats, the underlying etiology remains unknown. Pathological findings of adenomatous hyperplasia involving both thyroid lobes in most hyperthyroid cats suggests the possibility that feline hyperthyroidism may be similar to human Graves' disease, which results from high circulating levels of thyroid stimulating immunoglobulins (TSIs). To exclude high circulating levels of TSIs as the cause of feline hyperthyroidism, we measured intracellular concentrations of cyclic adenosine monophosphate (cAMP) in functioning rat thyroid cells (FRTL-5) incubated with IgG extracted from hyperthyroid cat serum. Since TSIs stimulate thyroid hormone secretion through activation of cAMP, their presence can be evidenced in vitro by generation of high cAMP concentrations in cultured thyroid cells. No significant difference was found in intracellular cAMP concentrations in FRTL-5 cells incubated with IgG from normal versus hyperthyroid cats. In contrast, IgG from a human patient with Graves' disease caused substantially more cAMP generation than either normal human IgG or IgG from the cats of this study. These results indicate that feline hyperthyroidism does not result from high circulating concentrations of TSI and, in that respect, is not analogous to Graves' disease.

Animals↗

PubMed1993

The effects of propranolol on skeletal muscle contraction, lipid peroxidation products and antioxidant activity in experimental hyperthyroidism.

1. The mean levels of lipid peroxidation products, namely conjugated diene and malonaldehyde, were increased in the soleus muscles of hyperthyroid cats, while the mean glutathione peroxidase activity was decreased. No corresponding similar changes were noted in the fast extensor digitorum longus muscles and serum. 2. Propranolol administration prevented the increase in conjugated diene level in the soleus muscles of hyperthyroid cat but not the malonaldehyde level. It also prevented the reduction in glutathione peroxidase activity in the slow oxidative soleus muscles of hyperthyroid cats. 3. Maximal twitch tension, subtetanic tension and maximum tetanic tension of soleus and EDL muscles were reduced in hyperthyroid cats. Propranolol administration for 5 weeks to hyperthyroid cats did not prevent the reduction in tension of contractions of these muscles. 4. It is suggested that lipid peroxidation might not be responsible for the myopathy in hyperthyroidism and propranolol administration does not improve skeletal muscle function in hyperthyroid animals.

Animals↗

PubMed1991

The effect of external calcium concentration on the negative inotropic action of dantrolene in isolated hyperthyroid and euthyroid heart.

The effect of altering external calcium concentration [Ca2+]o on the negative inotropic action of dantrolene was tested in Langendorff-perfused hearts from euthyroid and hyperthyroid rats. Elevated contractility was demonstrated in the hyperthyroid hearts at all the [Ca2+]o tested. At a [Ca2+]o of 1.25 mM (physiological), dantrolene (5 x 10(-5) M) significantly reduced contractility (dP/dtmax) in hyperthyroid but not in euthyroid hearts (-42% and -4% of zero-time values at 12 min perfusion, respectively). When hearts from both groups were paced at 375 beats/min, dantrolene again exerted a greater negative inotropic action in the hyperthyroid preparations, showing that the effect was not heart rate related. Elevating the [Ca2+]o did not further affect the time course of dantrolene action in hyperthyroid hearts. In euthyroid hearts, however, raising the [Ca2+]o to 2.5 and 3.75 mM caused a progressive increase in the negative inotropic action of dantrolene (-15% and -56% of zero-time values at 12 min perfusion, respectively). Our results demonstrate that dantrolene exerts a negative inotropic action which at physiological [Ca2+]o is greater in the hyperthyroid than in the euthyroid heart thus indicating that calcium handling by the myocardium is altered in the hyperthyroid state. However, dantrolene action in the rat myocardium is more complex than was at first believed; as in euthyroid hearts, its negative inotropic action appears to be increased rather than reduced by increases in [Ca2+]o.

Animals↗

PubMed1985

Trabecular bone remodeling and bone balance in hyperthyroidism.

In vivo tetracycline double-labeled iliac crest bone biopsies from 15 hyperthyroid patients were used for the reconstruction of curves describing the variation of resorption depth and formation thickness with time. The curves emerging were compared to curves reconstructed from 13 age- and sex-matched normal individuals (mean age 44 years). The median function period for resorptive cells in hyperthyroid patients (16 days) was about one-third the resorptive period in normals (51 days). No significant difference between the osteoclast-, mononuclear-, or preosteoblast-like cell resorption depths could be demonstrated between the two groups. Consequently, the median resorption rate in hyperthyroid patients (3.8 microns/day) was more than 3 times higher than the value in the control group (1.1 micron/day). Median Sigma, was shorter in the hyperthyroid group (109 days) than in the control group (151 days, P less than 0.05), as was the median initial mineralization lag time (5 and 16 days, respectively, P less than 0.01). No significant difference between the measured mean completed wall thickness (mcwT) values in the hyperthyroid groups and the control group could be demonstrated (58.1 and 60.5 micron respectively). Median initial mineralization rate in the hyperthyroid group (1.2 micron3/micron2 per day) was not significantly higher than the value calculated in the control group (0.9 micron3/micron2 per day), but median initial matrix appositional rate in hyperthyroid (4.8 microns3/micron2 per day) was 3 times higher than the value calculated for normals (1.6 micron3/micron2 per day) (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Oxidative changes and desialylation of serum proteins in hyperthyroidism.

BACKGROUND: Hyperthyroidism is associated with oxidative stress. Thyroid hormones are observed to influence the metabolism of plasma proteins. The present study was carried out to explore the level of sialic acid content and the oxidative changes of serum proteins in hyperthyroid subjects and matched healthy controls. METHODS: Blood was collected from 10 hyperthyroid patients and 10 age and sex matched healthy control subjects. The extent of carbonylation and desialylation of serum protein was estimated by dinitrophenylhydrazine and thiobarbituric acid methods, respectively. The protein cleavage and cross-linking were studied by separating serum protein in SDS-PAGE. The effects of in-vitro treatment of serum proteins with H(2)O(2) on the above-mentioned parameters were observed. RESULTS: The carbonylation was significantly higher and the sialic acid content was significantly lower in serum proteins of hyperthyroid cases in comparison to that of controls. Serum proteins were found to have increased levels of cleavage and cross-linking in hyperthyroid cases. The high molecular weight proteins were mostly cleaved. In-vitro treatment of serum proteins with H(2)O(2) led to similar changes. CONCLUSIONS: The study indicated that in hyperthyroidism, serum proteins undergo increased levels of oxidative changes leading to high turnover rate of blood proteins. A significant negative correlation between carbonylation and sialic acid content of serum proteins in hyperthyroidism and enhanced desialylation and carbonylation of serum proteins by in-vitro H(2)O(2) treatment suggest that oxidative stress can cause desialylation of serum glycoproteins.

Adult↗

PubMed2005

Simple electrocardiographic markers for the prediction of paroxysmal atrial fibrillation in hyperthyroidism.

BACKGROUND: Hyperthyroidism is a major cause of paroxysmal atrial fibrillation (AF). The purpose of this study was to evaluate the predictors of AF in the patients with clinical and subclinical hyperthyroidism. METHODS AND RESULTS: The study population consisted of four groups: group I (57 euthyroid healthy persons), group II (33 patients with subclinical hyperthyroidism), group III (69 patients with overt hyperthyroidism) and group IV (31 patients with overt hyperthyroidism and documented paroxysmal AF). The maximum P wave duration (P maximum) in group IV (114 +/- 8 ms) was significantly higher than group I (102 +/- 7 ms, p < 0.001), group II (106 +/- 7 ms, p < 0.001) and group III (108 +/- 9 ms, p0.005). The P wave dispersion (PWD) was measured as 46 +/- 9 ms in group IV and this was significantly higher than group I (29 +/- 8 ms, p < 0.001), group II (36 +/- 9 ms, p < 0.001) and grup III (38 +/- 8 ms, p = 0.001). The P maximum and PWD were higher in the patients with subclinical hyperthyroidism compared to healthy individuals. Univariate regression analysis revealed that age, P maximum and PWD, multivariate analysis showed that P maximum and PWD were significant predictors of paroxysmal AF. A PWD value of 37.5 ms separated group IV from others with a sensitivity of 90%, specificity of 85%, and positive predictive accuracy of 77%. CONCLUSION: Simply measuring P maximum and PWD values, we could identify the patients with high risk for the development of AF and these simple ECG parameters may help in clinical judgement to determine the requirement for treatment in the patients with subclinical hyperthyroidism.

Atrial Fibrillation↗

PubMed2006

Melatonin prevents oxidant damage in various tissues of rats with hyperthyroidism.

Impairment of thyroid functions brings about pathological changes in different organs of body. Findings of in vivo and in vitro studies indicate that thyroid hormones have a considerable impact on oxidative stress. Melatonin reduces oxidative damage through its free radical eliminating and direct anti-oxidant effects. The present study was undertaken to determine how a 3-week period of intraperitoneal melatonin administration affected oxidative damage caused in experimental hyperthyroidism in rat. The experimental animals were divided into 3 groups (control, hyperthyroidism, hyperthyroidism+melatonin). Malondialdehyde (MDA) and glutathione (GSH) levels were determined in different tissues. MDA levels in cerebral, liver and cardiac tissues in hyperthyroidism group were significantly higher than those in control and hyperthyroidism+melatonin supplemented groups (p<0.001). The highest GSH levels were observed in the group that was administered melatonin in addition to having hyperthyroidism (p<0.001). These results show that hyperthyroidism increased oxidative damage in cerebral, hepatic and cardiac tissues of rat. Melatonin supplementation may also suppress oxidative damage.

Animals↗

PubMed2007

Effect of experimental hypo- and hyperthyroidism on serum adiponectin.

Adiponectin, an adipocyte-derived hormone, has been shown to decrease body weight by increasing thermogenesis and lipid oxidation. Thyroid hormones have similar effects. Here we investigated if experimental hypo- and hyperthyroidism in rats would induce changes in serum adiponectin concentration. Adult rats became hypothyroid by treatment with 0.03% methimazole in the drinking water for 28 days or hyperthyroid by subcutaneous thyroxine injections (50 microg/100g body weight) for 10 days. Serum adiponectin level of hyperthyroid rats was 3.2-fold higher than that of euthyroid ones (P < .001), whereas that in hypothyroid rats tended to be lower (38%), but without statistical significance. Serum adiponectin had a positive correlation with serum thyroxine (r = .81, P < .001) and triiodothyronine (r = 0.68, P = .03) and a negative correlation with serum thyroid-stimulating hormone (P = -.62, r = 0.015). In addition, there was a negative correlation between serum adiponectin level and total visceral white adipose mass (= sum of inguinal, epididymal, and retroperitoneal depots; r = -0.43; P = .032), which was reduced by 40.5% in hyperthyroid (P < .01) but not in hypothyroid animals. A positive association between serum adiponectin level and brown adipose tissue mass was found (r = 0.43, P = .03), but not with body weight, which was reduced in both hypo- and hyperthyroid groups. Adiponectin has been reported to have an insulin-sensitizing effect. However, in hyperthyroid rats, higher serum adiponectin level was not accompanied by statistically different changes in basal serum insulin levels, blood glucose concentrations, or glucose tolerance as compared with euthyroid rats, except for a slight increase in blood glucose level at 120 minutes after glucose intraperitoneal administration (P < .05). Therefore, experimental hypothyroidism did not change serum adiponectin concentration, whereas hyperthyroidism induced an important elevation in the serum hormone concentration, with still unknown biological significance.

Adiponectin↗

PubMed2006

Thyroid disorders. Part I: hyperthyroidism.

The significant thyroid disorders that may be found in dental patients are presented in a series of 3 articles. This article (part I) deals with hyperthyroidism, part II with hypothyroidism and thyroiditis, and part III with neoplastic lesions of the thyroid. The signs and symptoms, laboratory tests used to diagnoses hyperthyroidism, and the medical management of patients with hyperthyroidism are presented in this paper. The dental management of patients with hyperthyroidism is discussed in detail. The dentist, by detecting the early signs and symptoms of hyperthyroidism, can refer the patient for medical diagnosis and treatment and avoid potential complications of treating patients with uncontrolled disease. These complications include the rare thyrotoxic crisis (thyroid storm) that may be precipitated by dental treatment, acute infection, or trauma in the patient with uncontrolled hyperthyroidism. Also, the use of epinephrine or other pressor ammines can cause a hypertensive crisis in the patient with uncontrolled hyperthyroidism. Patients will benefit from the early detection and referral by reducing the risks of the medical complications such as hypertension, cardiac arrhythmias, and congestive heart failure.

Antithyroid Agents↗

PubMed2002

Effect of ischemia-reperfusion on heart mitochondria from hyperthyroid rats.

OBJECTIVE: We investigated the effect of hyperthyroidism on the functional response of mitochondria to ischemia-reperfusion and its relationship with changes in mitochondrial susceptibility to stress conditions. METHODS: Hyperthyroidism was elicited by ten daily intraperitoneal injections of T3 (10 microg/100 g body weight). Mitochondria were isolated at 3000xg (M3) from homogenates of hearts perfused by the Langendorff technique after either 25 min reperfusion following 20 min ischemia or 45 min perfusion (controls). Rates of O2 consumption and H2O2 release with complex II-linked substrate, capacity to remove H2O2, extent of oxidative damage, levels of liposoluble antioxidants, such as ubiquinols and vitamin E, and susceptibility to Ca2+ -induced swelling were determined. RESULTS: During reperfusion, hyperthyroid hearts displayed a significant tachycardia together with a low functional recovery. In comparison to the respective controls, mitochondria from both euthyroid and hyperthyroid hearts subjected to ischemia-reperfusion protocol exhibited decreases in the rate of O2 consumption, capacity to remove H2O2, and concentration of antioxidants, and increases in the rate of H2O2 release, concentration of hydroperoxides and protein-bound carbonyls, and susceptibility to Ca2+ -induced swelling. Such changes were higher in mitochondria from hyperthyroid hearts. The increase in the protein percent content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000xg (M8) from hyperthyroid hearts after reperfusion, suggests that the decline of mitochondrial respiration of M3 fraction could be due to the degradation of the oldest, mature mitochondria endowed of high oxidative capacity, but low antioxidant capacity, which would be lost by heavy mitochondrial fraction and recovered in the light fraction. CONCLUSIONS: The higher susceptibility to ischemia-reperfusion of the heart from hyperthyroid animals is associated with a significant increase in mitochondrial dysfunction.

Animals↗

PubMed1996

Antioxidant status in experimental hyperthyroidism: effect of vitamin E supplementation.

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.

Animals↗

PubMed2001

Impaired neurogenic and endothelium-dependent relaxant responses of corpus cavernosum smooth muscle from hyperthyroid rabbits.

We investigated the effect of hyperthyroidism on the responsiveness of the rabbit corpus cavernosum smooth muscle. In male albino rabbits, hyperthyroidism was established by oral feeding of L-thyroxine at increasing dosages (150-450 microg/kg) over an 8-week period. This treatment produced a stable hyperthyroid state as indicated by the increased serum T4 levels. The reactivity of corpus cavernosum tissue from hyperthyroid animals and euthyroid control animals was studied in organ chambers. Hyperthyroidism caused impaired neurogenic and endothelium-dependent relaxant responses with decreased Emax and pD2 values. However, hyperthyroidism had no effect on both phenylephrine- and KCl-induced contractile responses and sodium nitroprusside- and papaverine-induced endothelium-independent relaxant responses, and there was no change in agonist potency. These data indicate that hyperthyroidism may impair both neurogenic and endothelium-dependent relaxation of corporal smooth muscle, and may contribute to the etiology of impotence.

Acetylcholine↗