The adrenosympathetic and adrenocortical function in cardiac insufficiency.

1960 
Levels of epinephrine, norepinephrine, 17-ketosteroids and total 17-hydroxycorticosteroids were determined in the urine, and both free and conjugated 17-hydroxycorticosteroids in the plasma, in 120 patients with cardiac insufficiency of different degrees, according to which they were divided into five groups. On the first hospital day, some patients gave assay values indicative of a distinct but transient adrenal medullary and cortical overactivity. In about one-fourth of our patients the excretion of epinephrine was augmented, especially in patients with insufficiency of medium severity (possibly as a result of hypoxic stress), whereas excretion was lowest in patients with the most severe insufficiency. Excretion of norepinephrine was augmented in only a few isolated instances. On an-average it was within normal limits. Except for a few elevated values, the free 17-hydroxycorticosteroids in the plasma were normal in the morning but approximately twice normal in the evening, indicative of a narrowed diurnal rhythm, especially in the patients with more severe insufficiency. This distribution remained fairly constant during the period of hospital observation. Cojugated 17-hydroxycorticosteroids in the plasma were generally normal with a narrow diurnal rhythm. In patients with most severe insufficiency some elevated morning and evening values were observed. These tended to become normal with treatment. The daily excretion of total 17-hydroxycorticosteroids in the urine was within normal range. 17-Ketosteroid excretion was low in accordance with the advanced age of most of the patients. There was no clear quantitative relationship between the substances assayed and the etiology, symptomatology, urinary volume, effectiveness of treatment and prognosis of the respective cases. Our results permit the assumption of a limited and temporary adrenal medullary over-activity in a minority of instances but they did not reveal any significant augmentation of adrenocortical activity in cardiac failure.
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