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Electroshock (2), surgical trauma (3), accidental trauma and acute illness (4) are associated with elevations in plasma-corticosteroids in man. It was of considerable interest to extend these observations to include adverse environmental conditions. Metabolic and hematologic changes similar to those resulting from the administration of adrenocorticotrophic hormone (ACTH) or corticosteroids have been reported to occur in human subjects experiencing hypoxia (5-7). In the present investigation blood ACTH and plasma corticosteroid concentrations were determined in subjects experiencing hypoxia, alone or in combination with heat. After 2, 15 or 45 minutes of exposure, 20 ml. of blood were drawn from an antecubital vein into a heparinized syringe for corticosteroid analyses, then 200 ml. were drawn directly into glacial acetic acid for ACTH analysis. Plasma corticosteroids were determined by the method of Sweat (8). Blood was processed by the oxycellulose technique (9) and assayed for ACTH in hypophysectomized rats by the adrenal ascorbic acid depletion method. (10). A dose of eluate equivalent to 40 ml. blood was injected into each of five test rats. An estimate of the concentration of ACTH was based on the average response of the test rats to doses of unknown and the responses induced by the administration of 1.0 and 0.25 milliunits (mU) U.S.P. ACTH per 100 Gm. rat on the same day. As an additional control, five hypophysectomized rats were injected with 0.9 per cent NaCl solution in each assay. Experiment 2. Three hour exposure; hypoxia induced by decompression in heated chamber. Five male subjects, 31 to 42 years of age, wearing shorts, were decompressed to the barometric pressure level equivalent to 14,000 feet altitude (total pressure, 446 mm. Hg; oxygen tension, 95 mm. Hg) in a chamber in which the air and wall temperatures were held at 510 C. and relative humidity at 13 per cent Air was circulated through the chamber at a constant rate, and the subjects remained seated throughout the exposure. Cardiovascular, respiratory, and body temperature determinations were made periodically, and 20 ml. blood samples (venous) for corticosteroid, hematocrit, sodium, and potassium determinations were drawn immediately before the exposure, at the end of the second and third hours of exposure, and one hour after exposure. Urine samples collected one hour after exposure were analyzed by standard methods (11) for uric acid, creatinine, sodium, and potassium, and comparison was made with samples obtained at the same 1642

Amino acid excretion was studied in young, healthy men during summer, fall and winter months in a southwestern U. S. location. Both untimed and timed urine samples were employed. The amino acids determined were alanine, arginine, cysteine, glutamic acid, glutamine, glycine, histidine, lysine, methyl histidine, serine, threonine and valine. Supplemental determinations included urine volume, creatinine, uric acid, urea, sodium and potassium. Using untimed urine samples and expressing values as ratios with creatinine, significant seasonal variation was found for alanine, arginine, cysteine, glutamic acid, glycine, lysine and serine. Submitted on April 11, 1959

No abstract

Balance studies were performed on a 16½-year-old white girl with hypomagnesemia due to celiac disease. During the initial phase of the study, a great magnesium loss in feces was demonstrated, with decreased magnesium excretion in urine and increased sodium and potassium retentions. Following the elimination of gluten in the diet, all mineral balances were restored to normal.