Western Society for Clinical Research 9’

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 forma- tion are apparent, many water-soluble, small- molecule components of the cell become radio- active. 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 ex- tracts of red cells, showed significant radio- activity and therefore were intermediates in the path of red cell glycolysis: glucose-l-phosphate, glucose-6-phosphate, fructose-6-phosphate, tri- ose-phosphate, diphosphoglycerate, hydroxyace- tic-phosphate, ribose-phosphate, adenylic acid, pyridine-nucleotide and at least two unidentified materials. The rapid labeling of ribose necessi- tates an amendment to current concepts of glycolysis. Of special interest was the high activity of the unique red cell compound, 2,3- di-phosphoglycerate. METABOLIC INTERRELATIONSHIPS BETWEEN

ACTH AND POTASSIUM. 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 ACTH- induced nitrogen loss in rats and diminishes ACTH-induced glycosuria in partially depan- creatized 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 ad- ministered both with and without simultaneous ACTH therapy.

Potassium in large doses administered con- currently with ACTH to arthritic patients fails to modify the anti-rheumatic and “nitrogen- wasting” 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 con- sistently occurs when ACTH therapy is initiated

JULY, 1952

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 sodium- retaining effects of ACTH.

Although potassium administration may mini- mize the hypokalemia due to acute administra- tion 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, Uni- versity of California School of Medicine, San Francisco, Calif. By intra-arterial catheterization of the liver,

kidney, spleen and lung, and with rapid arterio- graphic 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 aforemen- tioned concentrations. MECHANISMS OF DEGLUTITION, WITH REFERENCE

TO DISABILITY IN PATIENTS HAVING BULBAR-

PHARYNGEAL 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 degluti-

tion in patients having bulbar-pharyngeal poliomyelitis is that of weakness of the pharyn- geal constrictor musculature. Evaluation of this weakness is made difficult by its common as- sociation with weakness of the levator veli