Rolf Luft

TWO CASES OF POSTURAL HYPOTENSION SHOWING A DEFICIENCY IN RELEASE OF NOR-EPINEPHRINE AND EPINEPHRINE

Of the two forms of orthostatic hypotension, one, the arterial orthostatic anemia or hypotonic regulatory disturbance (1), is characterized by an increase in the pulse rate and a fall of the systolic blood pressure, with or without a rise in the diastolic pressure, upon change from the recumbent to the erect posture. These circulatory reactions are due to an increased activity of the sympathetic nervous system, which normally compensates for the hydrostatic displacement of blood due to the changes in position. In the second form, the postural hypotension or hypodynamic regulatory disturbance, this reaction of the sympathetic system to changes in posture is absent. The result is a momentary fall of the systolic as well as the diastolic blood pressure during a change from the recumbent to the erect posture, the pulse rate being maintained at a constant level (Figure 1). Postural hypotension was described for the first time in 1925 by Bradbury and Eggleston (2). It is a rather rare condition, of which Springarn and Hitzig (3), in 1942, found only 50 cases described in the literature. It is supposed to be due to organic lesions in the brain stem or spinal cord, following encephalitis, encephalomalacia and tumors,

The electrocardiogram and potassium metabolism during administration of ACTH, cortisone, and desoxycorticosterone acetate.

Abstract The electrocardiogram and the potassium metabolism were studied in cases of rheumatoid arthritis during administration of ACTH, cortisone and desoxycorticosterone acetate. ACTH protein (Li) was given in daily doses of 13 to 80 mg. for ten to twenty-two days, 200 mg. of cortisone per day was given for twenty-eight and seventy-six days, and desoxycorticosterone acetate in daily doses of 20 and 30 mg. for forty-three, sixty and thirty-four days. A significant decrease in the plasma potassium level to hypokalemic values was obtained. The change of intracellular potassium, not accounted for by changes in protoplasm, was not larger than 10 per cent of total body potassium. No typical hypokalemic electrocardiograms were observed. There was no correlation between changes in the electrocardiograms and the plasma potassium level.