Vasomotor reactions of visceral arteries to epinephrine

Western

Society for Clinical Research

radioactive carbon tagged glucose for periods giving approximately 50 per cent conversion of sugar to lactic acid. Although only- net glucose disappearance and equivalent lactic acid formation are apparent, many water-soluble, smallmolecule components of the cell become radioactive. The compounds labeled and their level of activity provide both a qualitative and quantitative picture of the metabolic route traversed by glucose carbon. The following substances, fractionated from trichloracetic extracts of red cells, showed significant radioactivity and therefore were intermediates in the path of red cell glycolysis: glucose-l-phosphate, glucose-6-phosphate, fructose-6-phosphate, triose-phosphate, diphosphoglycerate, hydroxyacetic-phosphate, ribose-phosphate, adenylic acid, pyridine-nucleotide and at least two unidentified materials. The rapid labeling of ribose necessitates an amendment to current concepts of glycolysis. Of special interest was the high activity of the unique red cell compound, 2,3di-phosphoglycerate. INTERRELATIONSHIPS

METABOLIC

BETWEEN

Leslie L. Bennett, Grant W. Liddle and Richard C. Bentinck, Metabolic Laboratory and the Divisions of Physiology and Medicine, University of California School of Medicine, Berkeley and San Francisco, Calif. It has been shown previously that feeding a diet high in potassium chloride prevents ACTHinduced nitrogen loss in rats and diminishes ACTH-induced glycosuria in partially depancreatized rats. This is a report of studies to determine how potassium might modify effects of ACTH in human subjects. Four arthritic patients were studied on a metabolic balance regimen and large doses of potassium salts (up to 36 gm. of potassium acetate per day) were administered both with and without simultaneous ACTH therapy. Potassium in large doses administered concurrently with ACTH to arthritic patients fails to modify the anti-rheumatic and “nitrogenwasting” effects of ACTH. Other effects of ACTH which are not modified by potassium include uric acid diuresis, eosinopenia, rise in fasting blood sugar and rise in 17-ketosteroid excretion. On the other hand, the effects of ACTH upon electrolyte metabolism are definitely modified by potassium. The sodium retention which consistently occurs when ACTH therapy is initiated ACTH

JULY,

1952

AND

POTASSIUM.

9’

is prevented or diminished by the concurrent administration of potassium. Superimposing potassium therapy upon an already established ACTH regimen induces prompt and marked diuresis of sodium. The marked sodium diuresis which ordinarily follows withdrawal of ACTH therapy may not occur in patients who have received potassium concurrently with ACTH. Potassium, therefore, inhibits the sodiumretaining effects of ACTH. Although potassium administration may minimize the hypokalemia due to acute administration of ACTH, the serious depletion of potassium which may result from prolonged treatment with ACTH can be repaired only with difficulty while ACTH treatment is continued. VASOMOTOR REACTIONS OF VISCERAL

ARTERIES

TO EPINEPHRINE. Howard R. Bierman, * Ralph L.

Byron, Jr., Rutherford Giljillan, Keith H. Kel& and Lauren5 White, Laboratory of Experimental Oncology, the Division of Medicine, University of California School of Medicine, San Francisco, Calif. By intra-arterial catheterization of the liver, kidney, spleen and lung, and with rapid arteriographic technics, it has been possible to observe the vascular patterns of these viscera in man. The introduction of various concentrations of epinephrine and its derivations produces specific changes in the vascular pattern of these organs. In general, the more rapid administration and the larger doses exerted more profound effects. In the spleen and liver, at uniform rates of administration, doses of 0.5 to 0.1 mg. of epinephrine causes the disappearance of small vessel pattern. Between 0.1 to 0.2 mg. the ma,jor arteries show diminution of caliber. Doses above 0.2 mg. cause complete spasm of the splenic artery with marked contraction of the hepatic artery. Renal and pulmonary arteries vary in their vasoconstrictor responses to the aforementioned concentrations. MECHANISMS OF DEGLUTITION, TO DISABILITY

WITH REFERENCE

IN PATIENTS HAVING BULBAR-

POLIOMYELITIS. ,Tames F. Bosma (introduced by Vincent C. Kelley), Department of Pediatrics, University of Utah, Salt Lake City, Utah. The critical factor in the disability of deglutition in patients having bulbar-pharyngeal poliomyelitis is that of weakness of the pharyngeal constrictor musculature. Evaluation of this weakness is made difficult by its common association with weakness of the levator veli PHARYNGEAL