The Production of Cardiac Hypertrophy by Thyroxine in the Rat

Sandler, Gerald; Wilson, G. M.

doi:10.1113/expphysiol.1959.sp001401

Cited by 36 publications

(6 citation statements)

References 6 publications

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“…Administration of thyroxine resulted in cardiac hypertrophy (Tables I, II). (23)(24)(25). In contradistinction to the heart, total body weight in the treated animals decreased (Table III).…”

Section: Resultsmentioning

confidence: 94%

The effect of thyroxine on lipid and carbohdrate metabolism in the heart.

Bressler¹,

Wittels²

1966

J. Clin. Invest.

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The administration of thyroxine to a number of experimental animals has resulted in marked structural and metabolic changes in the myocardium. Thyroxine has been shown to produce myocardial hypertrophy (1, 2) and to increase oxygen consumption and fatty acid utilization by the heart (3). In the dog made hyperthyroid by the administration of large doses of thyroxine, increased free fatty acid utilization by the heart was accompanied by a decreased uptake of glucose (3).In this communication data are presented which show that the administration of i-thyroxine to guinea pigs resulted in an increased rate of long chain fatty acid oxidation and a decreased rate of glucose oxidation by myocardial homogenates. The stimulatory effect on fatty acid oxidation was associated with elevated concentrations of free carnitine and acylcarnitines and increased long chain acyl coenzyme A (CoA)-carnitine acyltransferase (CAT) activity. The decreased glucose oxidation was associated with elevated levels of myocardial hexosemonophosphates and citrate. Citrate, the tissue concentration of which is increased by enhanced fatty acid oxidation, has been identified as one of several compounds that exert rate-controlling influences on glycolysis by inhibiting the activity of phosphofructokinase (PFK) (4, 5). Body weights were obtained before and after the thyroxine treatment was completed. The animals were then killed by a blow on the head. The entire heart was removed immediately, the great vessels were trimmed off at their origin, and the cardiac cavities were opened and freed of blood. The opened hearts were blotted on filter paper and weighed before further analyses were carried out.Hearts from treated animals and their controls used to assess the effect of thyroxine on total heart weight and on the concentrations of protein, ribonucleic acid, and deoxyribonucleic acid were homogenized in 8.0 ml of calcium-free Krebs-Ringer phosphate buffer, pH 7.4. The hearts used for enzymatic assays were placed in a volume of homogenizing medium such that their final protein concentrations were approximately equal.Protein concentration was measured by the biuret method (6). After completion of the biuret reaction the solution was filtered through a layer of Celite in a Buchner type funnel. This served to remove lipids, which produce turbidity of the solution. The results obtained by this procedure agreed closely with those obtained by Kjeldahl nitrogen determination (7).Analyses of myocardial DNA and RNA were done on trichloroacetic acid extracts of whole hearts. The p-nitrophenylhydrazine procedure of Webb and Levy (8) was used for DNA, and the orcinol method of Ceriotti (9) was used for RNA determination.The concentration of FFA in the myocardium was determined by the method of Dole as modified by Trout, Estes, and Friedberg (10). Quantification of triglycerides in the heart was done by the procedure of Van Handel and Zilversmit (11).Assays of palmitate, pyruvate, and glucose oxidations were carried out as previously described (12). Since the ...

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Section: Resultsmentioning

confidence: 94%

The effect of thyroxine on lipid and carbohdrate metabolism in the heart.

Bressler¹,

Wittels²

1966

J. Clin. Invest.

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“…However, other possible mechanisms ofaction include effects of T3 on cardiac myosin ATPase and Na+,K+-ATPase, as mentioned above. Thyroid has been reported to increase myocardial mass by inducing hypertrophy (34) and this could influence the heart's ability to increase cardiac output. However, the hypertrophy could be secondary to the increased work to which the heart is subjected.…”

Section: Discussionmentioning

confidence: 99%

Role of thyroid hormone in postnatal circulatory and metabolic adjustments.

1984

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At bstract. To assess the role of the early postnatal surge in plasma thyroid hormone concentrations on cardiovascular and metabolic adaptations, we measured cardiac output, total oxygen consumption, and plasma triiodothyronine (T3) concentrations in three groups of lambs in the first 6 h after delivery. 15 fetal lambs were prepared at gestational ages of 128-129 d by placing catheters in the brachiocephalic artery, descending aorta, distal inferior vena cava, left atrium, and pulmonary artery so that measurements could be made soon after delivery. They were divided into three groups: Group I comprised five control animals; Group II consisted of five fetuses in which thyroidectomy was performed at surgery at 129 d gestation; and Group III consisted of five animals in which thyroidectomy was performed at term gestation during delivery by caesarian section, prior to severing the umbilical cord. The lambs in Group I exhibited a rapid postnatal rise in T3 concentrations, similar to that described previously, reaching a peak value of about 5 ng/ml. Although the postnatal surge in T3 concentration was arrested in Group II and III animals, Group II had no detectable plasma T3, while the Group III animals had T3 concentrations of about 0.8 ng/ml, which were within the range previously reported for term lamb fetuses. The lambs in group II showed 40-50% lower left ventricular outputs (190 vs. 297 lambs in Group II also had significantly lower heart rates (131 vs. 192 beats/min) and mean systemic arterial pressures (56 vs. 72 torr). However, there were no significant differences for any of these measurements between the Group III and Group I lambs. The reduction in cardiac output in the Group II animals were reflected in a significantly lower blood flow to the peripheral circulation, but there were no significant differences in blood flow to other organs in the three groups. These studies indicate that plasma thyroid concentrations in the 2-3 wk prior to delivery and not the increase in thyroid hormone concentrations which occur after birth are important for postnatal cardiovascular and metabolic adjustments. We speculate that lack of circulating triiodothyronine in late gestation may affect postnatal cardiovascular adaptation by modifying normal beta adrenergic receptor development.

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“…This is true of thyroxine (Beznak, 1962;Edgren et al, 1976;Gemmill, 1958;Piatnek-Leunissen and Olson, 1967;Sandier and Wilson, 1959). There is considerable loss of body weight with administration of T 4 (Yazaki and Raben, 1975) which can lead to overestimation of the degree of cardiac hypertrophy through use of the heart weightto-body weight ratio.…”

Section: Discussionmentioning

confidence: 99%

“…This leads to increases in myocardial oxygen consumption and coronary blood flow in hyperthyroidism (Gunning et al, 1974;Leight et al, 1956;Piatnek-Leunissen and Olson, 1967;Skelton et al, 1970). Furthermore, the hyperthyroidism increases heart work, which leads to cardiac hypertrophy in many species, including man (Beznak, 1962;Edgren et al, 1976;Gemmill, 1958;Piatnek-Leunissen and Olson, 1967;Sandier and Wilson, 1959).…”

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confidence: 99%

Thyroxine-induced hypertrophy of the rabbit heart. Effect on regional oxygen extraction, flow, and oxygen consumption.

Talafih¹,

Briden²,

Weiss³

1983

Circulation Research

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SUMMARY. The effects of the administration of 0.5 or 1 mg/kg of 1-thyroxine for 3 or 16 days were studied in 55 New Zealand white rabbits. Heart size was 29% above control after 16 days of 1-thyroxine, despite lower body weights. In an anesthetized open-chest animal, regional microspectrophotometric observations of small arteries and veins to determine oxygen extraction were combined with regional blood flow measurements using radioactive microspheres to determine regional oxygen consumption by the Fick principle. Vascular flow reserves were studied through measurement of blood flow after the administration of chromonar HC1, 10 mg/kg. Myocardial oxygen consumption was, respectively, 2.4 and 3.8 times control after 3 and 16 days of 1-thyroxine. This was accompanied by significant increases in both coronary blood flow and oxygen extraction. In control, oxygen extraction and consumption were higher in the subendocardial region compared to the subepicardial area. No significant regional differences were found in flow, oxygen extraction, or consumption after 1-thyroxine administration. Chromonar increased coronary blood flow 2.8 times in the control animals, but did not significantly increase flow or decrease vascular resistance in the rabbits given 1-thyroxine. Adenosine increased coronary blood flow 3.5 times in the control animals but only 2.2 times in animals given 1-thyroxine for 3 days. Animals given 1-thyroxine had hypertrophied hearts with increased oxygen consumption, markedly increased flow, and increased oxygen extraction but without regional left ventricular differences. (Circ Res 52: 272-279, 19S3)

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The Production of Cardiac Hypertrophy by Thyroxine in the Rat

Cited by 36 publications

References 6 publications

The effect of thyroxine on lipid and carbohdrate metabolism in the heart.

The effect of thyroxine on lipid and carbohdrate metabolism in the heart.

Role of thyroid hormone in postnatal circulatory and metabolic adjustments.

Thyroxine-induced hypertrophy of the rabbit heart. Effect on regional oxygen extraction, flow, and oxygen consumption.

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