Abstract
The compound, 3,5,3[image]1-triiodothyronine was assayed in 4 patients with myxedema. The metabolic response to the daily admn. of 0.1 mg. of 1-triiodothyronine was 4-5 times that to admn. of an equivalent amt. of I-thyroxine. There were several qualitative differences between the effects of l-triiodothyronine and those of l-thyroxine. The protein-bound I in the blood of such patients following single intraven. doses or repeated daily doses of 1-triiodothyronine returned to myxedema levels in 16-36 hrs., which is in marked contrast to the slow disappearance of protein-bound I from the blood following I-thyroxine. Similarly, the basal metabolic rate returned to myxedema levels in 7-9 days after omission of triiodothyronine, as compared to 50-70 days after omission of thyroxine or thyroid. There is suggestive evidence that the excretion of I in the urine is greater after a single dose of triiodothyronine than after a single dose of thyroxine. These findings suggest that triiodothyronine is cleared rapidly from extracellular space, utilized in the cell with dispatch, and also leaves the intracellular fluid rapidly. Other clinical effects are produced more rapidly by triiodothyronine than by thyroxine. For example, the abnormal ecg. pattern in myxedema reverted to normal in several days after admn. of triiodothyronine; it takes several wks. or mos. for it to revert to normal following admn. of thyroxine or whole thyroid. It is suggested that thyroxine serves as a reservoir for the production of triiodothyronine. The latter is converted from thyroxine in tissues and may be the effective thyroid hormone.

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