Effects of Oral and Intramuscular Administration of Reserpine in Thyrotoxicosis

Canary, John J.; Schaaf, Marcus; Duffy, Benedict J.; Kyle, Laurence H.

doi:10.1056/nejm195709052571001

Cited by 155 publications

(20 citation statements)

References 28 publications

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“…In addition, they interact synergistically, and the effects of catecholamines are exaggerated by excess thyroid hormones and attenuated by thyroid hormone deficiencies (Waldstein 1966). Therefore, catecholamine depletion was previously considered a possible therapy for hyperthyroidism (Canary et al 1957), before it was found that it caused a high incidence of mental depression as a side effect (Buchanan et al 1959). Consistent with our a priori hypothesis, serum FT3 and FT4 levels were less suppressed under AMPT than they were under placebo treatment in the whole sample.…”

Section: Discussionsupporting

confidence: 76%

Neural correlates of free T3 alteration after catecholamine depletion in subjects with remitted major depressive disorder and in controls

2013

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RationaleThyroid hormones and their interactions with catecholamines play a potentially important role in alterations of mood and cognition. ObjectivesThis study aimed to examine the neurobiological effects of catecholamine depletion on thyroid hormones by measuring endocrine and cerebral metabolic function in unmedicated subjects with remitted MDD (RMDD) and in healthy controls. MethodsThis was a randomized, placebo-controlled, and double-blind crossover trial that included 15 unmedicated RMDD subjects and 13 healthy control subjects. The participants underwent two 3-day-long sessions at 1-week intervals; each participant was randomly administered oral α-methyl-para-tyrosine (AMPT) in one session (catecholamine depletion) and an identical capsule containing hydrous lactose (sham depletion) in the other session prior to a [18 F]-fluorodeoxyglucose positron emission tomography scan ( 18 FDG-PET). ResultsSerum concentrations of free T3 (FT3), free T4 (FT4), and TSH were obtained and assessed with respect to their relationship to regional cerebral glucose metabolism. Both serum FT3 (P = 0.002) and FT4 (P = 0.0009) levels were less suppressed after catecholamine depletion compared with placebo treatment in the entire study sample. There was a positive association between both FT3 (P = 0.0005) and FT4 (P = 0.002) and depressive symptoms measured using the MADRS. The relative elevation in FT3 level was correlated with a decrease in regional glucose metabolism in the right dorsolateral prefrontal cortex (rDLPFC; P < 0.05, corrected).Homan et al.2 ConclusionsThis study provided evidence of an association between a thyroid-catecholamine interaction and mood regulation in the rDLPFC.

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Section: Discussionsupporting

confidence: 76%

Neural correlates of free T3 alteration after catecholamine depletion in subjects with remitted major depressive disorder and in controls

2013

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“…The effects of isoproterenol on the individual heart rates, cardiac indexes, and mean arterial and mean right atrial pressures of three additional patients before, 10 minutes after intravenous infusion of 10 ml of isotonic saline solution, and 3 days after oral administration of nethalide placebos at intervals of 6 hours, are shown in Figures 3 and 4. Responses to isoproterenol after the placebos were similar to those obtained in the control period regardless of the route of administration.…”

Section: Resultsmentioning

confidence: 99%

Pharmacodynamic Effects of Beta-Adrenergic Receptor Blockade in Patients with Hyperthyroidism *

Wilson¹,

Theilen²,

Fletcher³

1964

J. Clin. Invest.

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The interrelationships of thyroid hormone, the adrenal medulla, and the sympathetic nervous system have been recognized since the early part of the present century (1-4). More recent studies of experimental hyperthyroidism by Brewster, Isaacs, Osgood, and King (5) 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 could be reversed by epidural block.Recent trials of reserpine (6, 7) and guanethidine (7-9) that release catecholamines and deplete the tissues of them have shown that these drugs can partially alleviate some clinical manifestations of thyrotoxicosis. 'The cardiac rate may be slowed, but consistent and significant reductions of the high cardiac output in patients with hyperthyroidism have not been reported, except by Goldstein, Furth, Becker, and Killip (10) using guanethidine. Methyldopa, a decarboxylase inhibitor, also slows the pulse rate of patients with hyperthyroidism, but does not significantly change the clinical manifestations (11), or reduce the elevated cardiac output or oxygen consumption (12). Furthermore, a continuous infusion of phentolamine (Regitine) in a hyperthyroid patient does not alter cardiac output (13), since it blocks alpha-rather than beta-adrenergic receptors. If the sympathetic nervous system is a crucial mediator of the hemodynamic changes in hyperthyroidism, it seems logical to explore the part that beta

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“…This tachycardia has been shown to involve all rhythmic elements of the heart (36) and is accompanied by an increased sensitivity to catecholamines (8,10) and a rise in myocardial oxygen consumption (37)(38)(39). It can be inhibited by the sympathetic blockade of epidural anesthesia (8), by reserpine (21,40) or guanethidine (22,23), and by complete heart block (41). It thus seems that the tachycardia of the hyperthyroid state is primarily due to adrenergic stimulation.…”

Section: Methodsmentioning

confidence: 99%

“…It is far more difficult to remove completely sources of catecholamines before testing the effect of thyroxine. Although many studies (17)(18)(19)(20)(21)(22)(23) have shown an inhibition of the response to thyroxine after removing or inhibiting catecholamines, most of these studies have failed to exclude completely the presence of catecholamines. Other studies (24)(25)(26)(27)(28) have failed to show any change in the effect of thyrox-* Submitted for publication June 7, 1963; accepted October 10, 1963. t Postdoctoral fellow of the National Science Foundation.…”

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confidence: 99%

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Studies on the Interactions of Thyroid Hormone and Catecholamines*

Bray¹

1964

J. Clin. Invest.

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Since the original demonstration by MagnusLevy (1) of the rise in respiratory exchange after feeding thyroid and the synthesis of thyroxine by Harington and Barger (2), the physiological effects of insufficient and of excess amounts of thyroid hormone have been well described (3). The cellular and biochemical mechanism by which thyroid hormones produce these effects is, however, still far from clear. Numerous studies have shown a direct effect of thyroxine on various in vitro systems (4), but these effects are often difficult to relate to the physiological effects of thyroid hormone.The resemblance of the symptoms of hyperthyroidism to the effects of sympathomimetic amines has given rise to the concept that the primary effect of thyroxine may be to alter the tissue sensitivity to epinephrine and norepinephrine. Substantial evidence, both clinical and experimental, has accumulated to support the idea that sensitivity to catecholamines varies directly with the intensity of action of thyroid hormone (5-16).Evidence for the converse hypothesis, i.e., that the tissue response to thyroxine is mediated by the action of catecholamines, is difficult to interpret. It is relatively easy to alter the state of thyroid activity and then test the response to catecholamines. It is far more difficult to remove completely sources of catecholamines before testing the effect of thyroxine. Although many studies (17)(18)(19)(20)(21)(22)(23) ine when catecholamines have been blocked by various pharmacological agents. Consequently the question of whether thyroxine acts only through its effects on catecholamines remains unsettled.In an effort to shed further light on this problem, studies using a combination of surgical and pharmacological techniques have been carried out. The effect of thyroid hormones and reserpine independently and in combination on thyroidectomized or thyroidectomized and adrenodemedullated rats has been investigated using metabolic rate, heart rate, and growth as indicators of response. MethodsMale rates of the hooded or albino strains from the Mill Hill breeding stock were used for thyroidectomy and adrenodemedullation, which was performed under ether anesthesia. Thyroidectomy was done through a mid-line incision (29), and to destroy any remaining thyroid tissue, 25 to 50 ,uc of I"8 was given 1 week after the operation. Adrenodemedullation, performed through bilateral flank incision at the same time as thyroidectomy, was done by mobilizing the adrenals and incising the capsule. The medulla and cortex were then removed from the capsule by gentle pressure on each side of the adrenal. Tap water was given postoperatively, since in our experience drinking water containing 0.9% sodium chloride did not alter survival. Animals were not used until at least 6 weeks after operation, at which time the hooded rats weighed 148 g and the albino rats 187 g, on the average. At the end of the studies on adrenodemedullated animals the adrenals were removed, homogenized in 10 ml of cold 5% trichloroacetic acid, and centrifuged. The ...

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Effects of Oral and Intramuscular Administration of Reserpine in Thyrotoxicosis

Cited by 155 publications

References 28 publications

Neural correlates of free T3 alteration after catecholamine depletion in subjects with remitted major depressive disorder and in controls

Neural correlates of free T3 alteration after catecholamine depletion in subjects with remitted major depressive disorder and in controls

Pharmacodynamic Effects of Beta-Adrenergic Receptor Blockade in Patients with Hyperthyroidism *

Studies on the Interactions of Thyroid Hormone and Catecholamines*

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