Thyroxine and Triiodothyronine Levels in Hyperthyroid Patients During Treatment With Propranolol

Harrower, A. D. B.; Fyffe, J. A.; Horn, D. B.; Strong, Judith A.

doi:10.1111/j.1365-2265.1977.tb02938.x

Cited by 50 publications

(16 citation statements)

References 13 publications

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“…This decreased 02 demand was accompanied by decreased myocardial flow and 02 extraction. The action of propranolol may be at the level of the [3-adrcnoceptor, however, there is some evidence to indicate that propranolol may also affect the metabolism of T4 by tissue (7).…”

Section: Discussionmentioning

confidence: 92%

Propranolol and thyroxine-induced hypertrophic rabbit hearts: Effect on heart size and regional O2 supply/consumption variables

Grover¹,

Houghton²,

Weiss³

1988

Basic Res Cardiol

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The purpose of this study was to determine the effect of acute and chronic propranolol on heart size and regional O2 supply/consumption variables in thyroxine (T4)-treated rabbit hearts. New Zealand white rabbits were given 0.5 mg/kg T4 for 3 or 16 days with and without concomitant 2 mg/kg propranolol. Another group was given 16 days of propranolol alone and another 3-day T4 group was given 2 mg/kg propranolol 1 h before the experiment began. Another group served as control. Myocardial blood flows were determined using radioactive microspheres and small arteriolar and venous O2 saturations were determined using microspectrophotometry. Treatment with T4 for 3 or 16 days increased the heart weight/body weight ratio, myocardial blood flow, and regional O2 consumption. 16-day T4 treatment resulted in myocardial flow 195% and O2 consumption 300% above control group values. When propranolol was given chronically along with T4, heart weight/body weight ratios did not increase to the degree seen with 3 or 16 days of T4, alone. Propranolol given acutely in 3-day T4-treated animals, resulted in a reduced O2 consumption and O2 extraction, though not to the extent seen with chronic propranolol treatment of T4-treated animals. Acute propranolol treatment slightly reduced myocardial blood flow in 3-day T4-treated animals, while chronic treatment significantly reduced it. Chronic propranolol treatment in 16-day T4-treated animals resulted in a significant reduction in flow and O2 consumption. Thus, T4 treatment increased O2 consumption, flow, and heart size and these effects could be attenuated using acute and chronic propranolol.

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Section: Discussionmentioning

confidence: 92%

Propranolol and thyroxine-induced hypertrophic rabbit hearts: Effect on heart size and regional O2 supply/consumption variables

Grover¹,

Houghton²,

Weiss³

1988

Basic Res Cardiol

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“…37 The drug probably acts similarly to non-thyroidal illness, either by alternative peripheral monodeiodination of thyroxine38 or by reduction in activity of the deiodinase enzyme activity responsible for tri-iodothyronine production.39 Though this may have important consequences in hyperthyroidism,40 it is unlikely to contribute to the acute effects of propranolol in hypothyroidism.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular function in hypothyroidism. Responses to exercise and beta adrenoceptor blockade.

Forfar¹,

Muir²,

Toft³

1982

Heart

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EdinburghSUMMARY The effects of exercise and beta adrenoceptor blockade on left ventricular function were assessed in eight patients with hypothyroidism before and during thyroxine replacement treatment. Left ventricular ejection fraction, measured by radionuclide ventriculography, was reduced in hypothyroid patients at rest and on exercise. The rise in ejection fraction with exercise was, however, similar in both groups. Pretreatment with intravenous propranolol reduced the ejection fraction at rest 9% in both hypothyroid and euthyroid patients and reduced the rise on exercise. Directional changes in a second index of myocardial contractility based on the shape of the ventricular volume curve paralleled the changes in the ejection fraction. Left ventricular function is therefore reversibly depressed by thyroid hormone deficiency but responses to exercise and beta adrenoceptor blockade are normal. There is no evidence of altered adrenergic sensitivity in the control of myocardial contractility in hypothyroidism.The clinical effects of varying thyroid function on the cardiovascular system have been recognised for many years. The mechanism of altered myocardial contractile function in hypothyroidism has, however, been less intensively studied. The bradycardia and cardiomegaly of myxoedema are familiar, and experimentally impaired myocardial contractility is well documented.

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“…Nevertheless, it is possible that higher doses of propranolol could alter the central inspiratory drive by blocking adrenergic action and by decreasing circulating T 3 [28]. In any case, 160 mg·day -1 propranolol only decreased T 3 levels in only ~5% of patients [33].…”

Section: Discussionmentioning

confidence: 99%

Regulation of breathing in hyperthyroidism: relationship to hormonal and metabolic changes

Pino-García¹,

García‐Río²,

Díez³

et al. 1998

Eur Respir J

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We sought to examine the breathing pattern, inspiratory drive and chemosensitivity of hyperthyroid patients and to explore the interactions between their thyroid hormones, basal metabolism and chemosensitivity. We studied 15 hyperthyroid patients and 15 sex- and age-matched controls. Thyroid hormone levels, arterial blood gas tensions, lung volumes, diffusing capacity for CO, maximal respiratory pressures and oxygen uptake measurements were performed. Breathing pattern and mouth occlusion pressure (P0.1), as well as ventilatory and P0.1 responses to hyperoxic progressive hypercapnia and isocapnic progressive hypoxia, were also evaluated. Compared with the control subjects, the hyperthyroid patients showed significantly lower resting arterial CO2 tension, tidal volume and significantly higher mean inspiratory flow and P0.1. Ventilatory and P0.1 responses to CO2 and hypoxia were also greater in the hyperthyroid patients than in the control group. All these changes returned to normal after treatment. In the patients, significant relationships between tri-iodothyronine and P0.1, P0.1 response to hypoxia, and P0.1 response to hypercapnia were found. In contrast, in hyperthyroidism there was no relationship between oxygen uptake and P0.1 response to hypoxia. We conclude that hyperthyroid patients exhibit a significant relationship between their thyroid hormone levels and their increased inspiratory drive and chemosensitivity.

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Thyroxine and Triiodothyronine Levels in Hyperthyroid Patients During Treatment With Propranolol

Cited by 50 publications

References 13 publications

Propranolol and thyroxine-induced hypertrophic rabbit hearts: Effect on heart size and regional O2 supply/consumption variables

Propranolol and thyroxine-induced hypertrophic rabbit hearts: Effect on heart size and regional O2 supply/consumption variables

Left ventricular function in hypothyroidism. Responses to exercise and beta adrenoceptor blockade.

Regulation of breathing in hyperthyroidism: relationship to hormonal and metabolic changes

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