The Hemodynamics of Thyrotoxicosis in Man With Special Reference to Coronary Blood Flow and Myocardial Oxygen Metabolism 1

Rowe, George G.; Huston, John H.; Weinstein, Arvin B.; Tuchman, Herman; Brown, John F.; Crumpton, Charles W.; Peterson, Audrey; Welch, Beryl; Fosshage, Phyllis

doi:10.1172/jci103273

Cited by 82 publications

(16 citation statements)

References 10 publications

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“…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: 81%

Mechanochemistry of cardiac muscle

Skelton¹,

Pool²,

Seagren³

et al. 1971

J. Clin. Invest.

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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,

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Section: Discussionsupporting

confidence: 81%

Mechanochemistry of cardiac muscle

Skelton¹,

Pool²,

Seagren³

et al. 1971

J. Clin. Invest.

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“…All workers who have examined the problem agree that both hypoand hyperthyroid heart muscle respond to the glycoside (5, [33][34][35]; however, analysis of the problem in patients and intact experimental animals is complicated by the facts that the absorption and the turnover of the drug (36), as well as the fraction of the cardiac output which enters the coronary circulation (37,38), may all be influenced by alterations in the thyroid state, making it difficult to deliver a known concentration of drug to the myocardium. In an earlier study from this laboratory it was observed that the percentage increase in contractile force of the right ventricle of intact hyperthyroid dogs was only slightly, though not significantly, lower than that observed in euthyroid animals (33).…”

Section: Mals (Figs 4 and 5)mentioning

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

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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.

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“…While cardiac parameters are invariably increased, as assessed by the shortening of systolic and diastolic time-intervals, the increase of systolic and diastolic function and the reduction in the left ventricular ejection fraction (3)(4)(5)(6), regional blood flow distribution is not uniform in hyperthyroidism. For example, blood flow in skeletal muscle, skin, cerebral, and coronary arteries is increased, whereas hepatic blood flow is unchanged (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography

Bogazzi

Bartalena

Brogioni

et al. 1999

European Journal of Endocrinology

122

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Objective: Thyroid blood flow is greatly enhanced in untreated Graves' disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). Subjects and methods:We investigated 24 normal subjects, and 78 patients with untreated hyperthyroidism (49 with Graves' hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto's thyroiditis, and 21 untreated hypothyroid patients with Hashimoto's thyroiditis. Results: Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8 Ϯ 1.2 cm/s. Patients with spontaneous hyperthyroidism due to Graves' disease, TSHoma, and toxic adenoma had significantly increased PSV (P < 0.0001, P = 0.0004, P < 0.0001 respectively vs controls) and CFDS pattern. Patients with Graves' disease had CFDS pattern II (mild increase of color flow doppler signal) in 10 (20%) and pattern III (marked increase) in 39 cases (80%). Mean PSV was 15 Ϯ 3 cm/s. Patients with toxic adenoma had CFDS pattern I (presence of parenchymal blood flow with patchy uneven distribution) in 2 (8%), pattern II in 16 (70%) and pattern III in 5 (22%). Mean PSV was 11 Ϯ 2.4 cm/s. Patients with TSHoma showed CFDS pattern I in one case (20%) and pattern II in 4 (80%). Mean PSV was 14.8 Ϯ 4.2 cm/s. Patients with thyrotoxicosis had normal PSV (4.2 Ϯ 1.1 cm/s in subacute thyroiditis, 4 Ϯ 0.8 cm/s in thyrotoxicosis factitia, P = not significant vs controls) and CFDS pattern 0. Untreated euthyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern 0, and mean PSV (4.3 Ϯ 0.9 cm/s; P = not significant vs controls). Untreated hypothyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern I in 14 cases (67%), pattern II in 4 (19%) and pattern 0 in 3 (14%) and mean PSV (5.6 Ϯ 1.4 cm/s) was higher than that of controls (P = 0.026). Conclusions: An increase in both intrathyroidal vascularity and blood velocity was observed in patients with spontaneous hyperthyroidism but not in thyrotoxicosis due to either ingestion of thyroid hormones or to a thyroidal destructive process. The slightly increased vascularity and blood velocity observed in patients with hypothyroid Hashimoto's thyroiditis suggests that thyroid stimulation by either TSH-receptor antibody or TSH is responsible for the increased thyroid blood flow.

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The Hemodynamics of Thyrotoxicosis in Man With Special Reference to Coronary Blood Flow and Myocardial Oxygen Metabolism 1

Cited by 82 publications

References 10 publications

Mechanochemistry of cardiac muscle

Mechanochemistry of cardiac muscle

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

Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography

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