ALBUMIN AFFECTS ERYTHROCYTE AGGREGATION AND SEDIMENTATION

Erythrocyte aggregation and sedimentation is determined by the concent ration of high molecular plasma proteins such as fibrinogen and immuno globulins. The role of albumin, the most abundant plasma protein, is c ontroversial. We analysed the influence of human albumin (0-80 g L(-1) ) on sedimentation behaviour of erythrocytes suspended (haematocrit 35 %) in fibrinogen-enriched normal plasma, plasma from patients with hyp oalbuminaemia, solutions of dextran 70 in buffer, and mixtures of fibr inogen, immunoglobulins and albumin in buffer. Sedimentation was measu red by the Westergren method, viscometry was performed at low and high shear rate. The addition of albumin to normal plasma, hypoalbuminaemi c plasma, or dextran solutions in buffer decreased the erythrocyte sed imentation rate. In contrast, in a mixture of fibrinogen and immunoglo bulins in buffer, albumin increased erythrocyte sedimentation. When ei ther fibrinogen or immunoglobulins were omitted, or fibrinogen was rep laced by dextran, albumin did not increase sedimentation, which indica tes that increased sedimentation was due to an interaction of all thre e compounds. The viscosity of erythrocyte suspensions was increased by albumin. It is concluded that the influence of albumin on erythrocyte aggregation is complex and depends on the technique used; low shear v iscosity is increased, but erythrocyte sedimentation, i.e. under no fl ow conditions, is decreased. The inhibitory action of albumin on the e rythrocyte sedimentation rate has clinical implications and must be kn own by physicians. It may help to interpret sedimentation rates more c orrectly and prevent misinterpreting-presumed therapeutic successes or failures.