Mechanism of Certain Abnormalities of the Circulation to the Limbs in Thyrotoxicosis*

Kontos, Hermes A.; Shapiro, William; Mauck, H. Page; Richardson, David W.; Patterson, John L.; Sharpe, Alton R.

doi:10.1172/jci105212

Cited by 38 publications

(10 citation statements)

References 17 publications

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“…This finding suggests that vasodilation might occur through mechanisms independent of beta-adrenergic receptors. It is known that the increase in cutaneous blood flow of the forearm in thyrotoxicosis is largely mediated by a cholinergic mechanism (16).…”

Section: Discussionmentioning

confidence: 99%

Effects of beta-adrenergic receptor blockade in normal subjects before, during, and after triiodothyronine-induced hypermetabolism.

Wilson¹,

Theilen²,

Hege³

et al. 1966

J. Clin. Invest.

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Adequate oral or intravenous doses of a betaadrenergic receptor-blocking drug, nethalide,' produce no significant changes in the resting oxygen consumption, heart rate, cardiac output, and systemic mean arterial or mean right atrial pressures of patients with spontaneous hyperthyroidism (1). These findings do not support the concept that the hemodynamic changes in hyperthyroidism are mediated through adrenergic stimulation of betaadrenergic receptors. The work of Brewster, Isaacs, Osgood, and King, however, supported the hypothesis that the sympathetic nervous system may be responsible for the metabolic and hemodynamic changes associated with the hypermetabolic state, since the alterations induced by thyroid feeding to dogs could be abolished by epidural blockade (2). The possibility exists that spontaneous hyperthyroidism and drug-induced hypermetabolism may have similar hemodynamic findings but different mechanisms. This study was designed to test the effects of beta-adrenergic blockade in normal subjects before, during, and after the induction of hypermetabolism with triio-

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Section: Discussionmentioning

confidence: 99%

Effects of beta-adrenergic receptor blockade in normal subjects before, during, and after triiodothyronine-induced hypermetabolism.

Wilson¹,

Theilen²,

Hege³

et al. 1966

J. Clin. Invest.

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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

125

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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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“…It is increased in hyperthyroidisml 1 and decreased in hypothyroidism. 6 The increased heat production is dissipated through the cutaneous circulation, which is also increased.6 In hypothyroidism, there are hemodynamic changes resulting from reduced cardiac output, increased peripheral resistance, and reduced blood volume.…”

Section: Introductionmentioning

confidence: 99%

Nailfold Capillaroscopy in Hypothyroidism and Hyperthyroidism: Blood Flow Velocity During Rest and Postocclusive Reactive Hyperemia

Pazos‐Moura

Moura²,

Breitenbach³

et al. 1998

Angiology

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Direct intravital microscopic examinations of nailfold capillaries were made in three groups of subjects: 15 healthy volunteers (C) and 11 patients, six with hypothyroidism (h) and five with hyperthyroidism (H). The groups h and H were examined twice, before the onset of treatment and when they returned to euthyroidism. Capillary blood flow velocity (CBFV) was measured during rest and after release of 60-second arterial occlusion. To assess autoregulatory capacity the authors determined peak CBFV postocclusion and time to reach it in single capillaries. In patients with hypothyroidism, before the onset of the treatment, the mean resting and the mean peak CBFV were significantly lower (resting CBFV-group C: 0.93+/-0.11 mm/s (mean+/-SE); group h: 0.33+/-0.09 mm/s; and mean peak CBFV-group C: 1.49+/-0.14 mm/s; group h: 0.79+/-0.19 mm/s). The time to reach mean peak CBFV postocclusion was significantly prolonged (group C: 8.9+/-0.65 s and group h: 19.2+/-2.0 s) compared with the group of healthy volunteers. When these patients achieved euthyroidism, all the studied parameters returned to control levels. In patients with hyperthyroidism only minor changes in CBFV could be detected. In patients with hypothyroidism, the skin microvascular autoregulatory mechanisms are disturbed. The impairments of the reactive hyperemia response could be correlated with the control of the disease (thyroid state).

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Mechanism of Certain Abnormalities of the Circulation to the Limbs in Thyrotoxicosis*

Cited by 38 publications

References 17 publications

Effects of beta-adrenergic receptor blockade in normal subjects before, during, and after triiodothyronine-induced hypermetabolism.

Effects of beta-adrenergic receptor blockade in normal subjects before, during, and after triiodothyronine-induced hypermetabolism.

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

Nailfold Capillaroscopy in Hypothyroidism and Hyperthyroidism: Blood Flow Velocity During Rest and Postocclusive Reactive Hyperemia

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