Perepdmaeenceese, « ae a tre ee ete ele gage Lee ae INJURY: ITs PATHOGENESIS AND THEEAPS Ta RADATION adrenals have been shown to phiy a role in the acute radiation syndrome, however, the importance of this role has received widely different evalus- tions. Certain similarities between adrenal cortical insufficiency and acute radiation injury. such as changes in blood chlorides. water metabolism, blood cholesterol, fat deposit in the liver and blood sugar have Leen claimed. There ix no doubt that polydipsia and polvurix follow heavy exposure, and that there may be a redistribution of fluids as indicated by blood volume, plasma and hematoerit changes, and some edemu. The changes in blood chemistry are small and apparently inconsistent. The fluid balance change> noted following acute totalbady exposure can be explained on the basis of vomiting and ‘or diarrhea, with the resulting fluid and elec- trolyte losses, as well as the eventual failure to eat and drink. Many of the changes may be explained as resulting from the stress accompanying the disease. Patt and associates have described a series of characteristic changes in the adrenals of the rat exposed to various dosages of x-radiation, which were prevented by hypophysectomy. Evidence has since been presented that indicates radiation is not an exception to the general rule that adrenalectomy sensitizes to all stresses (Cronkite and Chapman; Naplan). Nims and Sutton presented data on the rat which indicated that the polydipsia and decrease in adrenal cholesterol level following WBR were the result of increased activity of the pituitary-adrenal system, and that the initial fall in liver glycogen was principally the result of lowered food intake. Lasser and Stenstrom, in a clinical studyof patients following pelvic area irradiation, found the degree and time course of “radiation sickness” to correlate with changes in the absolute peripheral eosinophile count, but not with the Thorn ACTH-eosinophile, 4-hours response test. They concluded that the adrenal cortex underwent definite chatiges in the course of irradiation, but that the changes probably were not related to clinical “radiation sickness.” Santisteban e¢ al. showed that cortisone replacement therapy progressively restored the resistance of irradiated-adrenalectomized mice. However, events causing death in the irradiated-intact animals differed from those in the x-irradiated adrenalectomized group despite cortisone treatinent, indicating that cortisone may only partially restore resistance. Bond ef al. obtained highly selective irradiation of various small portions of the rat with a “pencil”? beam of 190 mev deuterons, and found that the thymus, spleen, and adrenal weights characteristic of pituitary-adrenal stimulation resulted only if and when theirradiation given imposed severe stress on the animal, as indicated by the gross symptoms of illness and body-weight loss. Such changes could not be elicited by irradiation of the adrenals alone, nor were they prevented by adrenal irradiation if additional radiation damage to other tissues sufficient to put the animal under ‘stress’? were present. The 5012684 fos? isolated, perfused calf’s adrenal gland was used to study the effects of