Blood Adrenocorticotrophic Hormone and Plasma Corticosteroids in men Exposed to Adverse Environmental Conditions12

Abstract

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

Adrenal Medullary Secretion During Hypoxia, Bleeding, and Rapid Intravenous Infusion

“…Our failure to find evidence of increased adrenal 17-OHCS output during hypoxia is in accord with the observations of Hale and associates, 19 who noted no increase in 17-OHCS levels in venous plasma of men exposed to moderate hypoxia.…”

A Possible Explanation for Cushing's Syndrome Associated With Adrenal Hyperplasia*

“…Using these methods, increased concentrations of ACTH have been demonstrated in the blood of patients with primary adrenal insufficiency and in some cases of the adrenogenital syndrome, but not in the blood of "unstressed" normal subjects (4, 5). Hale et al (12) estimated that intravenous infusions of ACTH at a rate as high as 6 i. u. per day would not lead to detectable concentrations of blood ACTH. In the present investigation 7 young men received infusions of ACTH at a rate between 1.5 and 5 i.u.…”

Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution

“…However, its contribution to the sympathoadrenal-mediated lymphocyte subset redistribution is not clearly defined (7,42). Induction of in vivo hyperthermia, by passive heat exposure (via hot-water immersion or hot-air exposure) or an exercise-induced increase in metabolism, is known to elicit significant neuroendocrine (20,34,41) and immune responses (8,10,15). Studies in which passive heating was used, in an attempt to isolate the immunologic effects of hyperthermia, demonstrate a pattern of leukocyte subset redistribution similar to that observed with exercise (12,15,28); however, the direction and magnitude of both hormonal and lymphocyte subset changes induced by passive heating are less consistent than those achieved by exercise (39).…”