Cardiac Failure in the Dog as a Consequence of Exogenous Hyperthyroidism

Piatnek-Leunissen, Dorothy A.; Olson, Robert E.

doi:10.1161/01.res.20.2.242

Cited by 53 publications

(24 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results have been reported from human skeletal muscle (20). These find- Previous attempts to define myocardial efficiency in hyperthyroidism have given conflicting results (21)(22)(23). In some instances myocardial efficiency has been thought to be increased (22,23 (25).…”

Section: Discussionsupporting

confidence: 80%

“…These find- Previous attempts to define myocardial efficiency in hyperthyroidism have given conflicting results (21)(22)(23). In some instances myocardial efficiency has been thought to be increased (22,23 (25). Although consistent with the hypothesis that thyroid hormone reduces the efficiency of energy utilization, these results were obtained under conditions which did not exclude possible alterations in the process of energy generation.…”

Section: Discussionmentioning

confidence: 64%

See 1 more Smart Citation

Mechanochemistry of cardiac muscle

Skelton¹,

Pool²,

Seagren³

et al. 1971

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T The possibility that alterations in the rate or efficiency of energy utilization could be involved in the control of cellular oxygen consumption by thyroid hormone was examined in right ventricular papillary muscles isolated from normal euthyroid cats and cats with experimentally induced hyperthyroidism and hypothyroidism. Energy production in the muscles was inhibited and isolated from the process of energy utilization by exposure to iodoacetic acid and nitrogen. After resting or performing variable amounts of contractile element work under isometric conditions, muscles were frozen, and the total amount of chemical energy (~P = creatine phosphate + ATP) used was determined. The resting rate of energy utilization in muscles from euthyroid animals was 0.78 ±0.07 tmoles/g per min of P.This rate was elevated in muscles from hyperthyroid cats to 1.00 ±0.09 gmoles/g per min and decreased in muscles from hypothyroid cats to 0.23 ±0.14 umoles/g per min. Isometrically contracting muscles from cats with hypothyroidism utilized only 64% as much energy as muscles from euthyroid cats while performing 81% as much contractile element work at a moderately decreased level of contractile state. Muscles from hyperthyroid cats utilized an average of 41% more energy than did muscles from euthyroid cats while contracting an identical number of times and performing an equal amount of contractile element work at a slightly increased level of contractile state. These results suggest that thyroid hormone directly influences the rate of cellular energy utilization. Furthermore, the increase in energy utilization in muscles from hyperthyroid cats could not be attributed entirely to observed alterations in contractile behavior, which indicates that excess thyroid hormone may decrease the efficiency of the conversion of cellular energy to work. However, the opposite effect, an increased efficiency of energy utilization, was not observed in muscles from hypothyroid cats. Thus, it is concluded that the calorigenic effects of thyroid hormone may be explained, at least in part, by alterations in the process of energy utilization. INTRODUCTIONThyroid hormone has many effects on cellular function, the most striking of which is its influence on oxygen consumption or energy metabolism. The stimulation of oxygen consumption found in most tissues after the administration of thyroid hormone has been attributed to changes in the rate of energy generation, the efficiency of energy generation, or a combination of these (1). The chief features of clinical and experimental hyperthyroidism and hypothyroidism have been postulated to result from changes in the process of energy generation (2), shown schematically in Fig. 1 as Coupling A. However, it is also possible that a change in the rate or efficiency of energy utilization, Coupling B,

show abstract

Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 64%

Mechanochemistry of cardiac muscle

Skelton¹,

Pool²,

Seagren³

et al. 1971

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…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%

“…Some of these effects may be direct and some may be related in part to interactions with catecholamines (Amidi et al, 1968;Margolius and Gaffney, 1965;Lee et al, 1965). 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).…”

mentioning

confidence: 99%

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

Talafih¹,

Briden²,

Weiss³

1983

Circulation Research

View full text Add to dashboard Cite

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)

show abstract

“…The recent development of methods for detailed and quantitative analysis of mechanical characteristics of isolated cat papillary muscle (8), removed from the nervous, humoral, and metabolic influences that exist in vivo, and the ability to compare the function of muscles obtained from different groups of animals (9), permit critical examination of these problems. In addition, although interpretation of many previous studies of myocardial high energy phosphate stores in altered thyroid states (10)(11)(12)(13)(14) was limited by the extreme lability of these energy stores, recent modifications of biopsy and analytic techniques have made possible the accurate assessment of these stores in vivo (15,16).…”

Section: Introductionmentioning

confidence: 99%

Influence of the Thyroid State on the Intrinsic Contractile Properties and Energy Stores of the Myocardium*

Buccino¹,

Spann²,

Pool³

et al. 1967

J. Clin. Invest.

377

100

View full text Add to dashboard Cite

Abstract. The intrinsic contractile properties of isolated cat papillary muscles and myocardial high energy phosphate stores were examined at three levels of thyroid activity and correlated with hemodynamic measurements in the intact animal. In addition, the relationship of thyroid state to endogenous norepinephrine stores and myocardial responsiveness to certain inotropic in-.terventions were studied. In muscles from hyperthyroid cats, the velocity of shortening and the rate of tension development were markedly augmented, while duration of active state was decreased, compared to euthyroid muscles. These findings occurred in the presence and absence of intact norepinephrine stores and over a wide range of temperature and contraction frequency. The opposite changes occurred in muscles from hypothyroid cats. Isometric tension was slightly higher in muscles from hyperthyroid and lower in muscles from hypothyroid cats. The inotropic response to both norepinephrine and strophanthidin varied inversely with the level of thyroid state and allowed all three groups of muscles to reach a common ceiling of isometric tension regardless of thyroid state. Creatine phosphate and adenosine triphosphate stores were intact at all three levels of thyroid state. Thus, the level of thyroid activity profoundly affects the intrinsic contractile state of cardiac muscle, independent of both norepinephrine stores and alterations in high energy phosphate stores, and, in addition, modifies the responsiveness of cardiac muscle to inotropic agents.

show abstract

Cardiac Failure in the Dog as a Consequence of Exogenous Hyperthyroidism

Cited by 53 publications

References 28 publications

Mechanochemistry of cardiac muscle

Mechanochemistry of cardiac muscle

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

Influence of the Thyroid State on the Intrinsic Contractile Properties and Energy Stores of the Myocardium*

Contact Info

Product

Resources

About