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Total red cell Ca2+ content and rheological determinants in a group of subjects with vascular atherosclerotic disease

G Caimi1, R Lo Presti, A Serra

  • 1Istituto di Clinica Medica e Malattie Cardiovascolari, Università di Palermo, Italy.

Microcirculation, Endothelium, and Lymphatics
|February 1, 1990
PubMed

Insights

Vascular atherosclerotic disease (VAD) alters red blood cell (RBC) microrheology, but not total calcium content. RBC calcium levels correlate with membrane polarization, not aggregation or fluidity in VAD patients.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biophysics

Background:

  • Vascular atherosclerotic disease (VAD) is a significant health concern.
  • Red blood cell (RBC) rheology plays a crucial role in microcirculation.
  • Altered RBC properties may contribute to VAD pathophysiology.

Purpose of the Study:

  • To investigate total red blood cell calcium (Ca2+) content in VAD patients.
  • To assess macro- and microrheological parameters in VAD.
  • To explore relationships between RBC Ca2+ content, rheology, and membrane properties.

Main Methods:

  • Evaluated total red cell Ca2+ content.
  • Assessed macro- and microrheological determinants.
  • Compared VAD subjects with healthy controls.
  • Utilized fatty acid probes to measure membrane polarization.

Main Results:

  • VAD subjects showed altered macro- and microrheological parameters compared to controls.
  • No significant difference in total red cell Ca2+ content was observed between VAD and control groups.
  • No correlation found between RBC Ca2+ content, blood cell volume (VBC), or mean erythrocyte aggregation (MEA) and membrane fluidity (Iex/Im ratio).
  • A correlation was identified between RBC Ca2+ content and the degree of polarization using fatty acid probes.

Conclusions:

  • RBC microrheological alterations are present in VAD.
  • Total RBC Ca2+ content is not significantly different in VAD patients.
  • RBC Ca2+ content correlates with membrane polarization, suggesting a potential role in VAD pathogenesis.

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