PLATELET-AGGREGATION IN RECOMBINANT-HIRUDIN-ANTICOAGULATED BLOOD

Recombinant hirudin (r-hirudin) inhibited the thrombin-induced aggregation and C-14-serotonin secretion of human platelets in the same concentration range as native hirudin. In r-hirudinized blood, lower spontaneous platelet aggregation was found than in citrated or heparinized blood. Except for a demonstrable aggregation-potentiating effect, adrenaline did not induce aggregation in r-hirudin- or in citrate-anticoagulated blood. The lowest platelet adhesion to glass surface was found in r-hirudinized plasma. The ADP-induced aggregation was nearly the same in the three differently anticoagulated plasma samples: however, desaggregation predominated in r-hirudinized plasma. Adrenaline caused only a slight aggregation in r-hirudinized plasma. ADP and adrenaline caused C-14-serotonin secretion in citrated plasma only. The collagen as well as the PAF- and arachidonic-acid-induced aggregation did not differ significantly in the three plasma samples. Hence, r-hirudin is suitable for studying platelet functions at physiological calcium concentrations.