[PP.12.15] THE POSSIBLE ROLE OF CHANGES IN THE PARAMETERS OF RED BLOOD CELLS IN PATHOGENESIS OF ISCHEMIC STROKE

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Abstract

Objective:

In recent years, the role of red blood cells (RBC) as both a deliverer of nitric oxide (NO), and a stimulator of NO release via RBC generated ATP has been widely discussed. In addition, an evaluation of the potential downstream effects of RBC-derived ATP, via its ability to stimulate NO in other cell types, was provided. Collectively, it is now apparent that the RBC is a determinant in functions other than oxygen delivery alone.

Objective:

We suggested that the changes in RBC parameters related to the above functions, could make a significant contribution to the development of ischemic stroke.

Objective:

The aim of this work was to study RBC parameters, the levels of the intracellular ATP, changes of the content of hemoglobin (Hb) complexes of patients with ischemic stroke (IS) for the identification of some pathogenic features of the disease.

Design and method:

Under supervision there were 552 patients (47,5+0,6 years old) with IS at sub-acute or residual stage, 30 healthy controls. The study of RBC properties was performed by dielectrophoresis, chromatography, 31P NMR spectroscopy. Changes in Hb complexes were investigated by Raman spectroscopy.

Results:

IS patients had marked disturbances of RBC deformability (low amplitude of deformation at the background of high summarized rigidity, viscosity), predisposing to the development of microcirculatory disorders and tissue hypoxia with a deficit of intracellular macroergs (2,3-DPG, alpha-, beta-, gamma-ATP) (p < 0,0001–0,05). These changes correlated with high levels of cholesterol fraction, an index of cholesterol/phospholipids in RBC membranes against decrease in total lipids, easily oxidable PHL, omega-3 index (p < 0,0001- 0,02). Probably the RBC ability to release reduced ATP in response to mechanical deformation, hypoxia, acidosis in IS patients will be very low. The levels of complexes Hb-NO (II) in IS patients were significantly lower than those in the controls (p < 0,0001), which reflected the decline reserves of erythrocyte NO and reduced discharge of O2.

Conclusions:

The revealed pronounced changes in RBC parameters contribute significantly to the pathogenesis of ischemic stroke and require different emphasis to be given to the course of therapy.

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