BACKGROUND: Blood banking procedures are associated with damage to red blood cell (RBC) membranes, which can impair their flow properties, namely, their deformability, aggregability, and adherence to endothelial cells (ECs) and thus possibly introducing a circulatory risk to recipients. This study was undertaken to comprehensively explore the effect of cold storage and gamma irradiation on RBC flow properties. STUDY DESIGN AND METHODS: RBC flow properties were monitored as a function of shear stress with a computerized cell flow properties analyzer. Because we had previously studied storage effect on RBC aggregability (Transfusion 1999;39:277-81), here we determined the storage effect on RBC adherence and deformability, by measuring them before (control) and during storage. Gamma irradiation effect on RBC aggregability, adherence, and deformability was determined before (control) and after irradiation. RESULTS: Cold storage significantly elevated the number of adherent RBCs and the strength of their interaction with ECs, and was marked by decreased RBC deformability as early as 2 weeks into the storage period. The elevation of RBC-EC interaction was well correlated with translocation of phosphatidylserine to the RBC surface. Gamma irradiation induced an immediate and marked increase in the number of rigid cells, but did not affect RBC adherence and aggregability. CONCLUSION: RBC flow properties appear to be especially sensitive to cold storage and gamma irradiation because they are impaired long before the expiration date. Because impaired RBC flow properties facilitate circulatory disorders, the potential circulatory risk of transfusion RBC with blood banking-impaired rheology should be considered.
Because blood transfusion is routinely given to patients with normal or high fibrinogen level, the transfusion of stored red cells has the potential to induce increased aggregation in vivo, depending on the storage period. This should be taken into account when blood transfusion is considered, particularly for patients with microcirculatory disorders.
To identify clinically relevant parameters of red blood cell (RBC) aggregation, we examined correlations of aggregation parameters with C-reactive protein and fibrinogen in unstable angina (UA), acute myocardial infarction (AMI), and bacterial infection (BI). Aggregation parameters were derived from the distribution of RBC population into aggregate sizes (cells per aggregate) and changing of the distribution by flow-derived shear stress. Increased aggregation was observed in the following order: UA, AMI, and BI. The best correlation was obtained by integration of large aggregate fraction as a function of shear stress. To differentiate plasmatic from cellular factors in RBC aggregation, we determined the aggregation in the presence and absence of plasma and formulated a "plasma factor" (PF) ranging from 0 to 1. In AMI the enhanced aggregation was entirely due to PF (PF = 1), whereas in UA and BI it was due to both plasmatic and cellular factors (0 < or = PF < or = 1). It is proposed that clinically relevant parameters of RBC aggregation should express both RBC aggregate size distribution and aggregate resistance to disaggregation and distinguish between plasmatic and cellular factors.
Therapeutic administration of immunoglobulins (Ig) has the potential to precipitate thrombotic events. This phenomenon may be explained by red blood cell (RBC) aggregation, which can be potentiated by Ig. The contribution of plasma albumin and fibrinogen to Ig-induced RBC aggregation is unclear. We examined RBC aggregation in three settings: 1) patients receiving therapeutic infusions of Ig; 2) patients receiving plasma supplemented in vitro with Ig; and 3) patients receiving RBC suspensions in standard buffer with varying concentrations of albumin, Ig, and fibrinogen. Ig infusion augmented aggregation of RBCs from patients with normal or high plasma levels of albumin but decreased aggregation in those with lower plasma albumin concentrations. In vitro, RBC aggregation was significantly increased only when all three components, fibrinogen, albumin, and Ig, were present at or above normal concentrations in the suspension but was unaffected when any one of the components was absent from the suspension. Our results suggest a three-way interaction among fibrinogen, Ig, and albumin that synergistically induces RBC aggregation in plasma. Understanding these interactions may help predict clinically important phenomena related to RBC aggregation, such as thrombotic complications of Ig infusion.
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