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February 2, 1957


Author Affiliations


From the Department of Medicine, Johns Hopkins University, and Medical Service of the Johns Hopkins Hospital.

JAMA. 1957;163(5):337-341. doi:10.1001/jama.1957.02970400009004

• Laboratory data from many different sources show that the rate of blood flow through various organs usually is not in proportion to their rate of oxygen consumption. The hemodynamic phenomena that accompany hyperthyroidism can therefore not be explained simply by saying that increased metabolic rate necessitates increased blood flow. The following hypothesis offers a more satisfactory explanation: The direct effect of the thyroid hormone in raising the metabolic rate is exerted mainly on such internal organs as the liver and kidney and to a lesser extent the voluntary muscles. Its effect in dilating the blood vessels of the skin is indirect and is really a response of the skin to the hyperthermia of the internal organs. The cutaneous vasodilation decreases the peripheral resistance in the vascular system; the heart then responds with a sufficient increase in rate to maintain a normal blood pressure within the aorta. This entails an increased volume of cardiac output per minute, increased rate of work by the heart, and ultimate embarrassment of the myocardium. In hypothyroidism, on the other hand, the initial change is a direct depression of the metabolic rate of the deep-lying organs; this lowers the body temperature, diminishes the need of radiation from the skin, results in cutaneous vasoconstriction, and so raises the peripheral resistance; in order to prevent a rise in the aortic blood pressure, the heart reduces its rate of output. Thus the circulatory system is confronted by the need of adjusting to imbalances of the thyroid hormone, and it reacts in ways that are sometimes beneficial, sometimes detrimental.