ISSN:
1432-1440
Keywords:
Cell volume
;
Na+/H+ antiporter activity
;
Human mononuclear leukocytes
;
Angiotensin-converting enzyme inhibitor
;
Diuretic therapy
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Previous studies in patients with congestive heart failure (CHF) treated with diuretics and/or digoxin have shown abnormalities of cellular volume and electrolytes in biopsies of skeletal muscle. These abnormalities seem to play an important role with regard to the dysregulation of peripheral vascular resistance and characteristic clinical features of CHF, for example, muscular weakness. This study assessed the effect of angiotension-converting enzyme (ACE) inhibitor therapy on cell volume and cell volume regulation in patients with CHF. Cell diameters of human mononuclear leukocytes (HML) were determined electronically by a Coulter Counter. Cell diameters for 19 patients with decreased left ventricular ejection fraction (determined via levocardiography) on therapy with ACE inhibitors (group 1) were compared to those of HML from patients on diuretics alone (group 2,n = 16). The activity of the Na+/H+ antiporter was determined by cell swelling in isotonic propionate. The control group consisted of 20 normal, age- and sex-matched volunteers. HML diameters were significantly increased from 7.16 ± 0.07 in normals to 7.24 ± 0.08 μm (group 1;P 〈 0.01) and 7.23 ± 0.11 μm (group 2;P 〈 0.05), indicating an abnormal regulation of cell volume. There were no statistically significant correlations between the individual ejection fraction or digoxin therapy and average cell diameters. In both patient groups ethylisopropylamiloride-sensitive swelling rates were normal compared to the control group indicating a normal activity of the Na+/H+ antiporter. In conclusion, increased cell sizes reflect a structural change in HML rather than a rapidly reversible functional abnormality which was not affected different by ACE inhibition and diuretic therapy. The pathomechanisms underlying abnormal cell sizes in CHF patients remain to be determined but could be similar to those responsible for muscular changes in CHF. Further studies should show whether HML, being easily accessible, are a valid cell model to reflect these muscular abnormalities in CHF, and whether a normal cell size can be achieved therapeutically by normalized neurohumoral activities.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00577741
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