Volumes and Na+/H+ antiporter activity of lymphocytes in patients with congestive heart failure

M Christ1, V Klauss, W Pliml

  • 1Medizinische Klinik, Klinikum Innenstadt, Ludwig-Maximilians-Universität, München, Germany.

The Clinical Investigator
|December 1, 1994
PubMed

Insights

Congestive heart failure patients show enlarged human mononuclear leukocytes (HML). Neither angiotensin-converting enzyme (ACE) inhibitor nor diuretic therapy normalized this cell volume abnormality, suggesting a structural change.

Area of Science:

  • Cardiology
  • Cell Biology
  • Pharmacology

Background:

  • Congestive heart failure (CHF) is associated with skeletal muscle abnormalities, including altered cellular volume and electrolytes.
  • These cellular changes may contribute to peripheral vascular resistance dysregulation and clinical symptoms like muscular weakness in CHF.
  • Previous treatments like diuretics and digoxin have been linked to these cellular abnormalities.

Purpose of the Study:

  • To investigate the impact of angiotensin-converting enzyme (ACE) inhibitor therapy on cell volume and its regulation in CHF patients.
  • To compare cell volume regulation in CHF patients treated with ACE inhibitors versus those on diuretics alone.
  • To assess potential structural versus functional changes in cell volume regulation.

Main Methods:

  • Measured electronic cell diameters of human mononuclear leukocytes (HML) using a Coulter Counter.
  • Compared HML from CHF patients on ACE inhibitors (n=19) with those on diuretics (n=16) and normal volunteers (n=20).
  • Assessed Na+/H+ antiporter activity via cell swelling in isotonic propionate, sensitive to ethylisopropylamiloride.

Main Results:

  • HML diameters were significantly increased in both CHF patient groups compared to normal controls (P < 0.01 for ACE inhibitors, P < 0.05 for diuretics).
  • No significant correlation was found between ejection fraction or digoxin therapy and average cell diameters.
  • Ethylisopropylamiloride-sensitive swelling rates were normal in both patient groups, indicating normal Na+/H+ antiporter activity.

Conclusions:

  • Increased HML size in CHF patients represents a structural cellular change, not a rapidly reversible functional abnormality.
  • Neither ACE inhibitor therapy nor diuretic therapy significantly altered this increased cell size.
  • Cell volume regulation, specifically Na+/H+ antiporter activity, appears preserved despite structural changes in HML.

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