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Timothy S. Harrison, MD; John H. Siegel, MD; William S. Wilson, MD; William J. Weber, MD

AMA Arch Surg. 1967;94(3):396-402.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THAT the clinical manifestations of hyperthyroidism depend upon the autonomic nervous system has been widely accepted since the experimental studies of Brewster et al¹ in thyroid-fed dogs. Clinical studies in primary hyperthyroidism on the effects of reserpine,² the effects of guanethidine,³ and on the response of the thyroid-treated subject to guanethidine⁴ have raised the question as to whether the effects of hypersecretion of thyroid hormone are due to a heightened sensitivity of effector organs to adrenergic stimuli or whether there is increased activity of the sympathetic nervous system as well. The recent studies of Horn-brook et al⁵ on the regulation of myocardial glycogen metabolism by thyroid hormone in rats suggest that thyroid administration produces a potentiation of catecholamine effects by causing an increased sensitivity of the myocardial catecholamine receptor site. This information plus that of DeGroot et al⁶ on the hyperkinetic circulation of resting . . . [Full Text PDF of this Article]

Author Affiliations
Ann Arbor, Mich

From the departments of surgery and medicine, the University of Michigan Medical School, Ann Arbor. Dr. Siegel is presently with the Department of Surgery. Albert Einstein Medical College, Bronx, NY. Dr. Weber is presently with the Department of Medicine, College of Human Medicine, Michigan State University, East Lansing, Mich.

Footnotes
Submitted for publication Sept 30, 1966.

Reprint requests to Department of Surgery, University of Michigan Medical School, Ann Arbor, Mich 48104 (Dr. Harrison).

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