Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with a toxic adenoma, already reduced in size by TSH, presented on the third day after treatment of a common cold by phenylpropanolomine, a severe pain in the thyroid gland. 4 weeks later, the nodule, which measured 3 x 4 cm. had clinically disappeared and the scan returned to normal. The disappearance 5 months later of the antithyroid antibodies confirmed the cure. Catecholamines, stimulating the production of thyroid hormone and producing temporary ischemia of the gland, phenylpropanolamine, a sympathomimetic drug, may have caused hemorrhagic necrosis of the adenoma and its disappearance.
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PMID:[Evanescent toxic thyroid adenoma. Possible role of phenylpropanolamine]. 20 Oct 31

1 The effects of thyroid state on the properties of adrenoceptors mediating inotropic and chronotropic responses of the rat heart were assessed on the basis of the relative potencies of alpha- and beta-adrenoceptor agonists, the effects of alpha- and beta-adrenoceptor antagonists and the tissue uptake of [3H]-phenoxybenzamine ([3H]-PB). 2 In isolated, electrically driven left atria the ratio of the inotropic potencies of isoprenaline and phenylephrine and the inhibitory potency of propranolol (40nM-4 muM) were significantly reduced after thyroidectomy and were moderately increased after thyroxine treatment of control rats. 3 Block of inotropic responses to noradrenaline and to phenylephrine by PB (7.3 nM-7.3 muM) and the tissue uptake of [3H]-PB were significantly greater in preparations from thyroidectomized than in those from control or from thyroxine treated rats. alpha-Adrenoceptor inhibition by phentolamine (0.26-2.6 muM) also increased after thyroidectomy, and phentolamine effectively protected alpha-adrenoceptors from block by and binding of [3H]-PB. 4 The beta1-receptor antagonist H 93/26 (0.1 muM) significantly potentiated alpha-adrenoceptor blockade by PB in hypothyroid but not in control preparations. 5 In spontaneously beating right atria the chronotropic potency of agonists and the effects of antagonists were altered in the same way as were inotropic responses and the slope of the agonist concentration-response curves were significantly reduced after thyroidectomy. Effects of agonists and antagonists were not significantly influenced by thyroxine treatment. 6 Changes in the effects and tissue uptake of sympathomimetic drugs observed after thyroidectomy were reversed to or beyond control levels by thyroid hormone treatment of thyroidectomized animals. 7 The results presented are interpreted as indicating a thyroid hormone-dependent interconversion of myocardial alpha- and beta-adrenoceptors. It is suggested that this interconversion is similar to that observed earlier in frog hearts at different temperatures, and that both effects may reflect an allosteric transition between two forms of a single basic structure.
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PMID:Thyroid hormone-dependent interconversion of myocardial alpha- and beta-adrenoceptors in the rat. 83 97

The acute (within hours) changes in the concentrations of T4, T3, reverse-T3 (rT3) and T3 resin uptake test (T3RU) were studied in 31 hyperthyroid patients for 4 h after po treatment with either acebutolol, oxprenolol, pindolol or timolol. In 21 of the patients, the changes were compared to changes in the serum concentrations of alpha 2-macroglobulin (a macromolecule) and two middle-sized molecules; thyroid hormone-binding globulin (TBG) and albumin in order to calculate the changes in extracellular distribution of the thyroid hormones and to distinguish between changes due to a changed metabolism and changes due to a changed distribution of the thyroid hormones. Acebutolol, oxprenolol and timolol caused a decrease in serum T3 after 1/2 h, and acebutolol and oxprenolol also a decrease in rT3 after 1/2 - 1 h, the changes reversed within 2 h. A concomitant decrease in serum albumin and TBG suggests a change in the extracellular distribution of middle-sized molecules to which thyroid hormones are attached, as an explanation of the acute decrease (1 h) of the thyroid hormones. The small and insignificant change in alpha 2-macroglobulin indicates that the changes are mainly extravascular, but the difference of alpha 2-macroglobulin changes between the drugs (acebutolol/timolol vs pindolol/oxprenolol) could depend on the intrinsic sympathomimetic activity of the drugs.
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PMID:Acute beta-blockade changes the extracellular distribution of thyroid hormones. 169 34

In a clinical study of 17 pregnant women treated with ritodrine, a beta-2-sympathomimetic agent used for tocolysis, thyroid hormone status was assessed longitudinally. This was done in order to verify the hypothesis that an increase in T3 levels could result from adrenergic stimulation, since propanolol, a beta blocking agent, has proved to decrease T3 levels in man. We have observed a significant increase in serum T3 concentrations 24-48 h after the start of the ritodrine treatment. The changes were only temporarely since one week after the start the serum T3 concentrations did not differ significantly from the pre-treatment levels. A decrease in T3 levels was found after discontinuation of treatment. No significant changes were found in T4 and TSH concentrations excluding an influence in ritodrine therapy on the pituitary-thyroid axes. It was concluded that stimulation of type I deiodinase was responsible for the changes in T3. These beta-2-mimetic variations may explain, to a certain degree, the unwanted chronotropic cardiac side effects of ritodrine and necessitates much care in using this therapy in hyperthyroidic patients.
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PMID:Effect of ritodrine on thyroid hormone concentrations. 365 57

In a clinical study of 17 pregnant women treated with ritodrine, a beta 2-sympathomimetic agent used for tocolysis, thyroid hormone status was assessed longitudinally. This was done in order to verify the hypothesis that an increase in T3 levels could result from adrenergic stimulation, since propranolol, a beta blocking agent, has proved to decrease T3 levels in man. Indeed, a statistically significant increase in T3 serum concentration and in T3/T4 ratio was found on the second day after the start of treatment with ritodrine (p less than 0.02 and less than 0.01 respectively). After discontinuation of treatment a decrease in T3 serum levels, compared to both treatment and pretreatment levels, was observed. The free T4 concentration showed a significant drop after the first week of treatment (p less than 0.01), but no changes were found in T4 and TSH levels. It was concluded that the beta 2-mimetic-mediated changes in thyroid status provide one more reason for restriction of the use of beta-mimetic drugs in hyperthyroidic patients and might offer an additional explanation for the undesirable chronotropic cardiac side-effects of the therapy.
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PMID:Changes in thyroid status in pregnant women treated with ritodrine. 366 69

Amiodarone, a powerful antiarrhythmic drug, likely exerts its major effect by antagonism of thyroid hormone (T3), probably at the receptor level. T3 is known to regulate beta-adrenergic receptor density in the heart but the effects of sympathomimetic drugs on thyroid hormone receptors (T3R) is not known. The aim of this study was to investigate how amiodarone and isoproterenol affect T3R-mRNA in cultured cardiomyocytes. Confluent, isoproterenol pretreated, AT-1 cardiomyocytes were treated with isoproterenol free medium, amiodarone, T3 and amiodarone together with T3 for 48 hours. Solution hybridization for the determination of mRNA for T3R alpha 1, alpha 2, beta 1 and beta 2 were performed. In itself isoproterenol upregulated T3R alpha 1, T3R beta 1, T3R beta 2 (p < 0.05), but did not affect the levels of T3R alpha 2. Amiodarone and T3, respectively, downregulated T3R alpha 1, T3R beta 1, T3R beta 2 (p < 0.05), but did not affect the levels of T3R alpha 2. Amiodarone and T3, added together, upregulated T3R alpha 2 and T3R beta 1 (p < 0.05) as compared to amiodarone or T3 alone. There was an antagonistic effect between amiodarone and T3 for the regulation T3R beta 1. This is the first evidence showing that amiodarone regulates T3R-mRNA concentrations during cathecholamine stress. Isoproterenol regulation of T3R-mRNA levels provides further evidence for the close interaction between the thyroid hormone and the beta-adrenergic systems.
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PMID:Downregulation of thyroid hormone receptor subtype mRNA levels by amiodarone during catecholamine stress in vitro. 759 31

Thyroid storm is an increasingly rare, life-threatening manifestation of thyrotoxicosis that can be precipitated by many physiologic stressors. The exact mechanism by which thyrotoxicosis decompensates into thyroid storm in certain individuals is unknown. These individuals may have an enhanced cellular sensitivity to either catecholamines or thyroid hormone. Serum levels of catecholamines are usually low or normal in thyrotoxic individuals. Ingestion of sympathomimetic drugs in thyrotoxic individuals may precipitate thyroid storm. This article presents an unusual case of Graves' disease that decompensated into thyroid storm after the ingestion of an over-the-counter cold medication containing pseudoephedrine.
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PMID:Case report: pseudoephedrine-associated thyroid storm: thyroid hormone-catecholamine interactions. 823 88

Retrograde ejaculation and hypothyroidism were diagnosed in a 19-mo-old Labrador retriever. The retrograde ejaculation was reversed following the administration of the sympathomimetic agent, pseudoephedrine hydrochloride, at a dose of 4 mg/kg per os given 1 and 3 h before semen collection. Antegrade ejaculation failed to occur after normalization of serum thyroid hormone levels by thyroxine supplementation. The pathophysiology of retrograde ejaculation is reviewed.
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PMID:Concurrent retrograde ejaculation and hypothyroidism in a dog: case report. 1672 15

Aim of the study was to investigate the status of thyroid homeostasis and the relationship between severe traumatic brain injury (TBI) and thyroid disorders. The study included 56 patients. Protocol of the study concluded: noninvasive and invasive hemodynamic monitoring, including PICCO, transcranial Doppler ultrasonography, measurement of intracranial pressure (ICP), indirect calorimetry, levels of thyroid stimulating hormone (TSH), T3, T4 and free fractions. Patients were divided into three groups. Group 1--with normal thyroid hormones (n = 20), Group 2--with the low T3 (n = 23) and Group 3 with the low T3 and T4 (n = 13). Correlation between the Glasgow Coma Scale (GCS) and thyroid hormone levels was obtained: the first group between GCS and T4 (r = 0.50), GCS, and free fraction T4 (r = 0.51); between the GCS and TSH (r = 0.51), T3 (r = 0.48) and T4 (r = 0.57) in the second group, and the third--with TSH (r = 0.67). Poor outcomes in the first group compound 15%, in the second group--39.2%, and in the third group--62.5% of patients. Doses of vasopressors were significantly higher in groups 2 and 3 compared with a first group. ICP was significantly higher in the group with the low T3 and T4. Development of intracranial hypertension correlated with the formation of thyroid insufficiency. Deficiency of thyroid hormones, especially the simultaneous reduction and T3, and T4 is associated with poor outcome in patients with severe TBI. Doses of sympathomimetic drugs used to optimize the parameters of systemic hemodynamics in acute severe head injury were higher in patients with deficiency of thyroid hormones.
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PMID:[Analysis of thyroid homeostasis disorders in patients with severe traumatic brain injury]. 2303 89

Takotsubo cardiomyopathy (TC) is a recently increasing diagnosed disease showed by transient apical or mid-apical left ventricular dysfunction. It is known as a disease of postmenopausal women, which is usually triggered by emotional or physical stress. Although the trigger is mostly endogenous, some drugs have also been reported as the cause. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine, and 5-fluorouracil. We present an unusual case of TC in which the possible trigger is ergotamine toxicity.
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PMID:Ergotamine-Induced Takotsubo Cardiomyopathy. 2509 82


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