Complement activation during storage of blood under normal blood bank conditions

During storage of CPD-A1 preserved whole blood factors of the
complement cascade become activated, as evidenced by a rapid
increase in the concentrations of C3a-desArg and C4a-desArg. After
10 to 14 days of whole blood storage, the elevations of C3a and C4a
levels were highly significant. This increase was paralleled by an
increase in the concentration of the lysosomal proteinase elastase
from polymorphonuclear (PMN) granulocytes. By contrast, the
concentration of the C3 activator complex C4b2b remained unchanged
even after 3 weeks of storage. The supplementation of the
anticoagulant CPD-A1 with the polyvalent-proteinase-inhibitor
aprotinin and the specific elastase- inhibitor eglin C failed to
inhibit complement activation, whereas leukocyte depletion could
partially abolish the increase of the concentration of C4a, but had
no effect on C3a concentrations. These observations support the
notion that cleavage of C4 during storage of whole blood is
partially leukocyte dependent, whereas the activation of C3 is
possibly caused by the activation of the alternate pathway of the
complement system by contact of plasma with plastic surfaces.