Title : The role of red blood cell as a participant in vasoregulation in the patients with ischemic stroke
The aim of the work was to assess the red blood cell (RBC) role as a participant in vasoregulation in the patients with ischemic stroke (IS) from two points: first, as a direct deliverer of NO and a stimulator of NO-release via RBC generated ATP.
Materials and methods. 467 patients (49,1+4,7 years old) with IS at its sub-acute or residual stage and 35 healthy controls were included into the study. The study of RBC properties was performed by dielectrophoresis, chromatography, 31P NMR spectroscopy. Changes in the content of Hb complexes were studied by Raman spectroscopy.
Results. IS patients had marked disturbances of RBC deformability (low amplitude of deformation at the background of high summarized rigidity, viscosity), RBC’s membrane characteristics (high electrical conductivity, low capacitance), low surface electric charge (reflected as the low dipole moment, the speed of RBC movement to electrodes) (p<0,0001-0,05), the last one correlated with the level of Von Wilebrand factor (r=0,72, p<0,033). These changes were associated 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).
We found low levels of intracellular macroergs (2,3-DPG, alpha-, beta-, gamma-ATP) in rigid RBC in IS patients than those in controls (p<0,0001-0,05). In patients with IS the content of the Hb-NO (II) complexes were sharply reduced (p<0,01-0,05), which led to a significant reduction in oxygen discharge and reflected the decline reserves of erythrocyte NO. Under hypoxic conditions as in the case of ischemic stroke, it is apparent that the RBC does release both ATP and NO. Is it possible that one of the molecules (ATP) is designed to stimulate NO in the endothelium, while the NO derived directly from the RBC has another function - to inhibit platelet aggregation in the presence of high levels of ATP being secreted by the RBC under hypoxic conditions. At the same time we revealed elevated levels of platelet aggregation with different types of inductors in patients with IS (p<0,01-0,02) as well as leukocytic-and-platelet aggregation (p=0,04). Probably the changed parameters of RBC in patients with IS contribute to the altered vasoregulation.
Conclusion. The decline reserves of intracellular NO, macroergs in rigid RBC in patients with ischemic stroke has been revealed. This fact as well as altered release of these compounds, associated with low deformability of RBC, may lead to modified vasoregulation in ischemic stroke.