It is generally believed that the alterations in total body oxygen consumption which accompany functional disturbances of the thyroid gland reflect widespread metabolic changes in all cells and tissues (1, 2). Numerous studies have identified some of the tissues that participate in the over-all disturbance of metabolic rate. For example, in zitro, kidney, liver, heart, and skeletal muscle tissues of animals previously treated with thyroid substance or thyroxine display increased oxygen consumption (3-7), whereas kidney, liver and muscle of thyroidectomized animals show lower than normal oxygen consumptions (5, 8). In man, Myers, using the bromsulphalein method, found the splanchnic oxygen consumption in hyperthyroidism to be elevated out of proportion to the total body metabolic rate, although the splanchnic blood flow remained essentially unchanged (9).In the case of the metabolic rate of the brain, in vitro studies have yielded controversial results. Cohen and Gerard (10) have found considerably higher than normal rates of oxygen consumption in minced brain tissue of rats made hyperthyroid by the administration of thyroid substance. Similar results have been obtained by MacLeod and Reiss (11) who administered thyrotropic hormone following hypophysectomy. On the other hand, no such increases were found by Spirtes (12) or by Gordon and Heming (6), and Fazekas and associates (13) could find no difference from normal in the cortical oxygen consumption of both hyperthyroid and hypothyroid rats.Studies of the effect of desiccated thyroid substance on the cerebral metabolic rate of human subjects suffering from cretinism were made by Himwich and co-workers ( 14 tric flow recorder and cerebral arterio-venous oxygen differences, they found marked increases in cerebral blood flow and cerebral oxygen consumption following thyroid administration. Only relative changes could be measured by this method, however. By means of the nitrous oxide method, quantitative determinations of cerebral blood flow and oxygen consumption in patients with hyperthyroidism have failed to demonstrate any significant differences from normal young men (15)(16)(17). On the other hand, in myxedema, a markedly reduced cerebral blood flow and metabolism and an elevated cerebral vascular resistance have been reported by Scheinberg and associates (18). Recently, Madison, Sensenbach and Ochs (19) have reported the results of a similar study on four hyperthyroid and four myxedematous subjects, the latter studied both before and after therapy. Using as normal controls the values obtained when the myxedematous subjects were made euthyroid by treatment, they failed to find in untreated myxedema the decrease in cerebral metabolic rate described by Scheinberg, although the circulatory findings were essentially the same. In their hyperthyroid group, however, in contrast to the previous studies of Sokoloff and his coworkers (15,16) and Scheinberg (17), Madison and coworkers (19) found the cerebral blood flow to be significantly elevated compared to that in ...
