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It is commonly known that red blood cell (RBC) tendency to reversibly aggregate contribute to the unique flow properties of blood. The fibrinogen-induced aggregation is primarily based on non-specific processes. Nevertheless, recent investigations disclosed a possibility of the specific fibrinogen-RBC binding, however, its role in RBC aggregation remains unclear. We conducted a study to determine whether this specific interaction is essential for natural RBC aggregation. The influence of glycoprotein (GP) IIb-IIIa inhibitor, monafram, on RBC aggregation was compared in RBC suspensions and in whole blood samples from healthy volunteers and, in addition, from patients with systemic lupus erythematosus (SLE) using laser-light backscattering detection and optical tweezers. The effect of monafram on normal RBC aggregation was detectable only in the early phase of intercellular interactions and it involved a deceleration of the aggregation, which was equally expressed in native blood samples and RBC suspensions based on platelet-free plasma. Additionally, in SLE patients, monafram weakened the strength of paired RBC aggregates in platelet-free suspensions. In healthy subjects, strengthened aggregates were found mainly in platelet-containing bulk RBC suspensions. These findings suggest that normal specific fibrinogen-RBC binding could lead to early accelerated formation of RBC aggregates, which could increase possible beneficial effects of reversible RBC aggregation. The strength of RBC aggregates could be modified by platelets in normal subjects and by specific fibrinogen-RBC binding in SLE patients.

Glycoprotein IIB-IIIA inhibitor, monafram decelerate the early phase of red blood cells aggregation