Search

1. Using Hg203labeled mercaptomerin sodium and studying radioautographs and renal distribution, 91.7% of an intra-muscularly injected dose of 1 mg Hg/kg was found in the kidney within the first hour, and maximum concentration occurred in the cortical area. 2. Radioactivity was detected for 28 days in plasma and in renal tissue. 3. Intravenous administration of radioactive mercaptomerin sodium resulted in a rapid decline in plasma concentration during the first 5 minutes. Rate of urinary excretion appears to be a function of arterial plasma-renal vein plasma difference.

1. Thiopental influences thyroid metabolism primarily by depriving the thyroid of available I2.2. The prolonged inhibition of thyroid activity by thiopental is probably related to accumulation of its metabolic products in the thyroid.

A method for determining ion transportation through the mucosa of the urinary bladder is described. This method has been used on normal and artificially constructed bladders in dogs.Rapid and continuous absorption of iodide, sodium and phosphorus ions takes place through the mucous membrane lined bladders, while only minimal amounts of these ions are absorbed through the normal bladder and through bladders constructed by means of seromuscular grafts.

1. A new concept is described for the intracavitary use of radiocobalt employing an agent to precipitate the cobalt directly on the mucosa of the urinary bladder together with dispersing agent to enhance penetration of the radiocobalt into the tissues. 2. Results in the use of this technic in dogs are presented. When 8-oxyquinoline solution was instilled into the bladder prior to the radiocobalt, there was an increase and prolongation of measureable radioactivity. When both 8-oxyquinoline and sorbitol were used this effect was further augmented.

The carcinogen, 2-acetylaminofluorene, produced a riboflavin deficiency in rats, reducing the liver riboflavin below control values. Increasing the riboflavin content of the diet prevented the appearance of the deficiency, keeping the liver riboflavin at normal levels. In the absence of protein in the diet, however, the increased riboflavin did not prevent the development of the deficiency.