The role of the adrenal cortex in the pathogenesis of ascites has been studied in adrenalectomized clogs with thoracic inferior caval constriction. Discontinuation of hormone therapy resulted in a diuresis which demonstrates that adequate adrenocortical function or replacement therapy is essential for ascites formation during normal sodium (Na) intake. Evidence is presented in support of the thesis that sodium retention results from an excess of circulating adrenocortical salt-retaining hormones.dogs with ascites, (2) data on the efficacy of DCA in producing the characteristic pattern of urinary and fecal electrolyte excretion in adrenalectomized dogs with thoracic inferior caval constriction, and (3) observations during the diuresis which followed removal of the caval ligature in the same animals.
METHODSStudies were conducted on four trained female mongrel dogs weighing 16 to IS Kg. Right adrenalectomy was performed before the thoracic inferior vena cava was constricted to produce ascites. The animals were then studied for a three to four week control period. Subsequently, the left adrenal gland was removed and observations were made during an experimental period of several months. Later, the caval ligature was removed and studies made during recovery. Dogs 1 and 2 were observed during all phases of the study but dogs 3 and 4 were studied only during administration of DCA to produce the pattern of electrolyte excretion which occurs in dogs with ascites and intact adrenal glands.Determinations were made in the postabsorptive state and before daily hormone administration. The experimental procedures and chemical methods have been described previously 2 ' 3 ; in addition, ascitic fluid volume was measured by T-1S24 dye dilution.The dogs were fed a synthetic diet containing SO Calories per kilogram per day, 0.6 Gm. per kilogram per day of nitrogen and either 2 or 4 mEq. per kilogram per day of Na; K intake was 17.6 mEq. per day. Intake was constant during each experiment. Water was allowed ad libitum
muscularly only to 17 patients. In addition, sulfadiazine was used in all but 1 of the cases and the specific rabbit serum was administered to 17 patients and aureomycin to 1 patient. Of the 90 patients, 87 recovered and 3 died, a recovery rate of 96.6 per cent. The 17 patients treated with intramuscular but without intraspinal injections of streptomycin recovered completely. With regard to the adjunctive therapy, it was difficult to evaluate the role of sulfadiazine. There was no evi¬ dence that rabbit serum played a contributory role. There were relatively few toxic reactions in the series, and neurologic residua occurred in a small number of the cases. Several important problems require further investigation, particularly those pertaining to the occur¬ rence of sequelae and the method of choice in strepto¬ mycin therapy.
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