Background:

Eryptosis, the suicidal erythrocyte death leads to cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptotic erythrocytes adhere to the vascular wall by binding of phosphatidylserine to the CXC chemokine ligand 16 (CXCL16). At least in theory, the binding of suicidal erythrocytes to the vascular wall could trigger thrombosis. As thrombosis is fostered by dehydration, the present study explored the possibility that dehydration influences eryptosis.

Materials and methods:

Plasma osmolarity was determined by a vapor pressure method, plasma ADH, aldosterone and 1,25(OH)₂D₃ utilizing respective ELISA or radioimmunoassay kits, plasma plasma Ca²⁺ by photometry. Annexin V-binding was utilised to identify phosphatidylserine exposuing erythrocytes, forward scatter to analyse cell volume, Fluo 3 fluorescence to estimate cytosolic Ca⁺² activity, a perfusion chamber to quantify adherence of erythrocyte to HUVEC under dynamic conditions.

Results:

A 36 hours dehydration was followed by significant increase in plasma osmolarity as well as plasma ADH, aldosterone, 1,25(OH)₂D₃ and Ca⁺². The dehydration triggered cell shrinkage and increased cytosolic Ca²⁺ activity, phosphatidylserine exposure as well as the percentage of erythrocytes adhering to HUVEC under flow conditions at arterial shear rates.

Conclusions:

The present observations demonstrate that dehydration increases eryptosis, followed by increased adhesion of erythrocytes to the vascular wall.