Advertisement
Research Article| Volume 76, ISSUE 3, P383-390, September 1970

A defect of red blood cell potassium transport in acute myocardial infarction

  • Mario F. Villamil
    Correspondence
    Reprint requests: Mario F. Villamil, M.D., Mount Sinai Hospital, 8720 Beverly Blvd., Los Angeles, Calif. 90048.
    Footnotes
    Affiliations
    From the Cedars-Sinai Medical Research Institute and the Division of Medicine, Cedars-Sinai Medical Center Los Angeles, Calif. U.S.A.

    From the Department of Medicine, University of California Los Angeles School of Medicine Los Angeles, Calif. U.S.A.
    Search for articles by this author
  • Valeria Rettori
    Affiliations
    From the Cedars-Sinai Medical Research Institute and the Division of Medicine, Cedars-Sinai Medical Center Los Angeles, Calif. U.S.A.

    From the Department of Medicine, University of California Los Angeles School of Medicine Los Angeles, Calif. U.S.A.
    Search for articles by this author
  • Elbert F. Simpson
    Affiliations
    From the Cedars-Sinai Medical Research Institute and the Division of Medicine, Cedars-Sinai Medical Center Los Angeles, Calif. U.S.A.

    From the Department of Medicine, University of California Los Angeles School of Medicine Los Angeles, Calif. U.S.A.
    Search for articles by this author
  • Charles R. Kleeman
    Affiliations
    From the Cedars-Sinai Medical Research Institute and the Division of Medicine, Cedars-Sinai Medical Center Los Angeles, Calif. U.S.A.

    From the Department of Medicine, University of California Los Angeles School of Medicine Los Angeles, Calif. U.S.A.
    Search for articles by this author
  • Author Footnotes
    ∗ Established Investigator, American Heart Association.
      This paper is only available as a PDF. To read, Please Download here.

      Abstract

      The ouabain-sensitive (OS) and ouabain-insensitive (OI) K uptake and K content of red blood cells (RBC) were measured in 23 normal subjects, in 10 patients with myocardial infarction (MI) in the acute stage and after subsidence of acute symptoms, and in 13 patients with acute noncardiac diseases. Total and OS K uptake were lower (p < 0.05 and p < 0.001) in patients during the acute stage of MI (1.68 and 0.99 mEq. per kilogram of wet weight per hour) than in normal subjects (1.95 and 1.44 mEq. per kilogram of wet weight per hour) and increased in all MI patients after subsidence of acute symptoms (1.98 and 1.49 mEq. per kilogram of wet weight per hour, p < 0.02 and p < 0.0025). The abnormality was unrelated to drugs or associated diseases. Low values of OS K uptake were also found in 5 patients with acute noncardiac diseases. Two of these patients had acute hepatitis, one had status asthmaticus, and two were in the early postoperative stage. RBC K content was not significantly different in the 3 groups. Changes in K content paralleled changes in OS K uptake in only half of the patients with MI. The K transport defect is not specific for acute MI, and more than one mechanism may be involved.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Translational Research
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Welt L.G.
        • Sachs J.R.
        • McManus T.J.
        An ion transport defect in erythrocytes from uremic patients.
        Trans. Ass. Amer. Physicians. 1964; 77: 169
        • Welt L.G.
        • Smith E.K.M.
        • Dunn M.J.
        • Czerwinski A.
        • Proctor H.
        • Cole C.
        • Balfe J.W.
        • Gitelman H.J.
        Membrane transport defect: the sick cell.
        Trans. Ass. Amer. Physicians. 1967; 80: 217
        • Villamil M.F.
        • Rettori V.
        • Kleeman C.R.
        Sodium transport by red blood cells in uremia.
        J. Lab. Clin. Med. 1968; 72: 308
        • Cunningham Jr., J.N.
        • Carter N.W.
        • Rector Jr., F.C.
        • Seldin D.W.
        Transcellular membrane potential in human skeletal muscle. A study of membrane depolarization accompanying severe illness.
        Clin. Res. 1969; 17: 83
        • Glynn I.M.
        Sodium and potassium movements in human red cells.
        J. Physiol. 1956; 134: 278
        • Smith T.W.
        • Butler Jr., V.P.
        • Haber E.
        Determination of therapeutic and toxic serum digoxin concentrations by radioimmunoassay.
        New Eng. J. Med. 1969; 361: 1212
        • Grahame-Smith D.G.
        • Everest M.S.
        Measurement of digoxin in plasma and its use in diagnosis of digoxin intoxication.
        Brit. Med. J. 1969; 1: 286
        • Binnion P.F.
        • Morgan L.M.
        • Stevenson H.M.
        • Fletcher E.
        Plasma and myocardial digoxin concentrations in patients on oral therapy.
        Brit. Heart J. 1969; 31: 636
        • Anderson N.B.
        The effect of local anesthetic and pH on sodium and potassium flux in human red cells.
        J. Pharm. Exp. Ther. 1968; 163: 393
        • Dunn M.J.
        The effect of transport inhibitors on sodium outflux in red blood cells.
        Clin. Res. 1968; 16: 565
        • Hoffman J.F.
        • Kregenow F.M.
        The characterization of new energy-dependent cation transport processes in red blood cells.
        Ann. N. Y. Acad. Sci. 1966; 137: 566
        • Lubowitz H.
        • Whittam R.
        Ion movements in human red cells independent of the sodium pump.
        J. Physiol. 1969; 202: 111
        • Hoffman J.F.
        • Kregenow F.M.
        The characterization of new energy-dependent cation transport processes in red blood cells.
        Ann. N. Y. Acad. Sci. 1966; 137: 566
        • Smith E.K.M.
        • Samuel P.D.
        Abnormalities in the sodium pump of erythrocytes from patients with hyperthyroidism.
        Clin. Sci. 1970; 38: 49
        • Campion D.S.
        • Lynch L.J.
        • Rector F.C.
        • Carter N.
        • Shires G.T.
        Effect of hemorrhagic shock on transmembrane potential.
        Surgery. 1969; 66: 1051