230 /. /. Christian 



on metabolic processes may reflect a primary action at one biochemical site, 

 possibly on cytochrome c (Rawson et al., 1955). Sollman (1957) has listed 

 the following additional effects of thyroxine. Increased levels of thyroid 

 hormones usually are accompanied by an increased pulse rate, increased 

 nervous excitability, weight loss, and decreased liver glycogen. Thyroxine 

 also sensitizes the tissues, especially the blood vessels, the actions of 

 sympathomimetic compounds such as epinephrine (see above) as well as 

 to the toxic effects of poisons. The increased sensitization apparently occurs 

 at the receptor mechanisms. Thyroxine also effects the circulation, but 

 mainly as a result of increased heat production. Thyroxine has a direct 

 effect on the heart in increasing its oxygen consumption, but it also has an 

 indirect effect on the heart and the rest of the circulatory system in the 

 following way. The delayed, indirect, effect is due to an increased metabolic 

 demand of the tissues which results in an increase in carbon dioxide and 

 decreases in oxygen at the arteriolar level. These effects result in a subse- 

 quent decrease in peripheral resistance, increased venous return, and, via 

 cardiac reflexes such as the Bainbridge, an increased cardiac output and 

 increased pulse pressure. The increased heat resulting from increased oxida- 

 tion must be dissipated, and this is accomplished by dilatation of the vessels 

 and opening of the arteriovenous anastomoses in the skin and other tissues 

 with an accompanying increase in the amount of heat loss due to radiation. 

 The normal calorigenic action of the thyroid hormones is essential for 

 normal growth, maturation, and tissue differentiation. 



Proper functioning of the thyroid and the production of thyroid hormones 

 is completely dependent on an adequate dietary intake of iodine. Inorganic 

 iodine is essential for the formation of the thyroid hormone by the thyroid 

 gland, as the thyroid is incapable of trapping organic iodine (Salter, 1949; 

 Halmi et al., 1953; Rawson et al., 1955) . The way in which trapped inorganic 

 iodide and tyrosine are converted into the thyroid hormone (s) has been 

 critically reviewed by Rawson et al., (1955). Inorganic iodide is trapped 

 and presumably momentarily oxidized to active iodine in the thyroid epi- 

 thelium. Pituitary thyrotropic hormone promotes the trapping of iodide 

 by the thyroid gland, although the gland has some autonomy in this ac- 

 tivity (Vander Laan and Greer, 1950; Halmi et al., 1953; Vander Laan and 

 Caplan, 1954; Vander Laan, 1955). The trapped and activated iodine is 

 then used in converting tyrosine to diiodotyrosine, probably in the presence 

 of peroxidases and cytochrome oxidases. Two molecules of diiodotyrosine 

 are condensed to form a single molecule of thyroxine (tetraiodothyronine), 

 which combines with thyroid globulin (thyroglobulin) and is stored as 

 such in the colloid of the thyroid follicles. Other iodinated thyronines are 

 found in the thyroid, but in much smaller amounts than thyroxine. These 

 probably result from partial iodination and may represent other pathways 



