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C Symons

Publications and source records attributed to C Symons.

At least 19 recordsLinked to original sources
PubMed1988

The importance of membrane stabilization in protecting the developing rat myocardium from the actions of triac.

Administration of triiodothyroacetic acid (triac) to pregnant rats produces cardiac hypertrophy and myofibrillar disarray in the hearts of the newborn offspring. Previous experiments have shown that concurrent administration of dl exprenolol or dl or d propranolol prevent the disarray but not the hypertrophy, suggesting that membrane stabilization and not beta-adrenergic blockade may be responsible for modifying the actions of triac. In order to clarify this, further experiments have been carried out whereby timolol, a beta-blocking agent with minimal or no membrane stabilizing activity, and procainamide, a pure membrane stabilizing compound, have been administered with triac. Timolol had no effect, but procainamide reduced the level of disarray and the hypertrophy to a minor degree. The results have thus confirmed the proposal that membrane stabilization is of major importance in modifying the actions of triac.

Animals↗
PubMed1985

Role of calcium in the induction of cardiac hypertrophy and myofibrillar disarray. Experimental studies of a possible cause of hypertrophic cardiomyopathy.

The role of calcium in the pathogenesis of hypertrophic cardiomyopathy was investigated experimentally. For this purpose the calcium antagonist verapamil and the calcium ionophore A23187 were administered to pregnant rats together with triac in order to observe their effect on triac induced myocardial disarray and hypertrophy in developing rat hearts. At a low dose verapamil reduced both the level of disarray and hypertrophy, but a higher dose produced hypertrophy when given alone. A23187 did not appreciably potentiate the actions of triac when given in combination but when administered alone produced both disarray and hypertrophy. Verapamil prevents the inward movement of calcium ions to the myocardial cell, whereas A23187 increases the inflow of calcium ions. The results suggest that the actions of triac in producing myocardial disarray and hypertrophy are attributable to an increased concentration of intracellular calcium.

Animals↗
PubMed1985

Cardiac hypertrophy, hypertrophic cardiomyopathy, and hyperparathyroidism--an association.

Left ventricular hypertrophy (symmetric, asymmetric, or hypertrophic cardiomyopathy) is an almost invariable accompaniment of primary hyperparathyroidism. Five of 18 patients with hypertrophic cardiomyopathy had raised serum concentrations of parathyroid hormone with normal serum calcium concentrations. Left ventricular hypertrophy did not occur in any of the six patients with hypercalcaemia alone. These relations suggest that parathyroid hormone rather than a rise in the extracellular calcium concentration is associated with a spectrum of left ventricular hypertrophy. All patients with increased circulating parathyroid hormone concentrations should have echocardiographic examination of the left ventricle. Conversely, parathyroid hormone concentrations should be measured in all patients with left ventricular hypertrophy from an unknown cause, especially those with hypertrophic cardiomyopathy.

Adult↗
PubMed1983

Effect of triac and beta-adrenergic blocking agents on the myocardium of developing rats.

Triiodothyroacetic acid, triac, when given to rats during pregnancy, causes hypertrophy and intracellular disarray in the hearts of their offspring and concurrent treatment with dl propranolol can prevent the latter abnormality. Further experiments have been carried out to test the effect of dl oxprenolol and d propranolol on triac-induced myofibrillar disarray. Administration of dl oxprenolol at the same time as triac prevented disarray but a higher dose than that of dl propranolol was required to produce this effect. Disarray was also prevented by d propranolol. Selective consideration of the membrane stabilising, beta blocking and agonist activities of dl oxprenolol and d and dl propranolol leads to the conclusion that although direct or indirect beta stimulation by triac may play a small part in its disruptive effect on the developing myocardium, its main deleterious action can be blocked by membrane stabilisation.

Animals↗
PubMed1981

Production of cardiac muscle abnormalities in offspring of rats receiving triiodothyroacetic acid (triac) and the effect of beta adrenergic blockade.

As a part of a continuing study on the effects of thyroid hormones on heart muscle, triiodothyroacetic acid (triac), either alone or concurrently with propranolol, has been administered to rats during pregnancy. Control groups received either buffer or propranolol. Offspring, which were given no further treatment, were killed at intervals after birth and their hearts examined histologically, histochemically, and electron microscopically. At 2, 6, and 14 days, offspring of triac-treated rats showed cardiac hypertrophy and, at ultrastructural level, marked disarray of the myofibrils was present. By 28 days, arrangement of the myofibrils had become regular but hypertrophy persisted and was still found in rats examined at 56 days of age, after which time the myocardium was normal. Offspring of rats which had received propranolol at the same time as triac showed a similar pattern of hypertrophy but myofibrillar disarray was not found. Propranolol alone produced no abnormalities. These findings provide further evidence that thyroid hormone analogues can adversely affect heart muscle. When considered in conjunction with previous experiments which showed that thyroxine or triac cause severe hypertrophy but not disarray when given directly to growing rats, they suggest that thyroid hormones can produce a spectrum of abnormalities, thought to depend on the stage of myocardial development at which the stimulus is administered. In the present experiment, the triac-induced myofibrillar disarray but not the hypertrophy was prevented by propranolol, indicating that beta-adrenergic blockade or some other action of propranolol protects the developing myofibrils. Possible mechanisms for the adverse effects of thyroid hormones and the protective action of propranolol are discussed.

Animals↗
PubMed1978

Response to thyrotrophin-releasing hormone in atrial dysrhythmias.

Seventy-eight clinically euthyroid patients with atrial dysrhythmias, either established or paroxysmal, and sixty-three patients in sinus rhythm with coronary disease were screened for hyperthyroidism using thyroid function tests including the thyroid-stimulating hormone (TSH) response to thyrotrophin-releasing hormone (TRH). All had normal levels of serum thyroxine (T4) apart from three with dysrhythmias who were found to have hyperthyroidism. Twenty per cent of patients with atrial dysrhythmias and 10% of those in sinus rhythm had exaggerated TSH response to TRH. Thirty-six per cent of patients with an exaggerated response of TSH to TRH had significant titres of thyroid auto-antibodies compared with 15% with positive antibodies in those with normal TSH response to TRH. Auto-immune thyroid disease may be more closely related to heart disease than has previously been recognized. Rapid atrial dysrhythmias may occur in the presence of a normal serum thyroxine, high levels of TSH and positive thyroid antibodies.

Adult↗
PubMed1977

Thyroid and heart.

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Coronary Disease↗
PubMed1977

Effect of triac on the developing heart.

Triac (diethanolamine salt of triiodothyroacetic acid) was administered by intramuscular injection to 12 pregnant female rats. These were divided into a control group and three other groups, each receiving different doses of triac. The effect of triac on the hearts of their offspring was studied morphologically. Histological examination showed evidence of only mild hypertrophy, but ultrastructurally, disarray of myocardial fibrils and other changes similar to those observed in patients with hypertrophic cardiomyopathy were found in the litter of the group receiving the highest dose. It is suggested that thyroid function should be studied in patients with obscure cardiac disease.

Animals↗
PubMed1975

The production of cardiac hypertrophy by tri-iodothyroacetic acid.

Severe cardiac hypertrophy has been produced experimentally in rats by long-term, low-dose treatment with tri-iodothyroacetic acid. The dose used was insufficient to cause any apparent systemic or metabolic effect. It is suggested that similar iodinated substances in the blood in man, resulting from normal or abnormal thyroid hormone catabolism, may be causally related to some forms of cardiomyopathy.

Acetates↗