Platelet counting detects lesser degrees of platelet aggregation than conve
ntional aggregometry. In order to prevent progressive platelet aggregation
or disaggregation after sampling it is customary to fix blood samples. Howe
ver fixation may introduce other artefacts. We first compared stability of
platelet counts in EDTA-, citrate- and r-hirudin-anticoagulated blood from
healthy volunteers. Second, the stability of platelet counts in unfixed EDT
A- and hirudin-anticoagulated blood was compared with glutaraldehyde-fixed
blood in the same anticoagulants. Third, the effect of in vivo heparin admi
nistration on platelet counts in EDTA- and hirudin-anticoagulated blood was
studied. Platelet counts within 2 h of collection were significantly highe
r in EDTA- than in hirudin- or citrate-anticoagulated blood (P=0.002 vs. hi
rudin and P=0.001 vs. citrate). Twenty-four hour counts in hirudin and EDTA
were unchanged (P=0.3 and P=0.2, respectively, vs. earlier counts), Counts
in citrate increased significantly (P=0.007; n=10), Platelet counts in fix
ed blood did not differ significantly from those in unfixed blood. Heparin
administered for cardiopulmonary bypass reduced platelet counts in hirudin-
anticoagulated blood from (mean +/-1 standard deviation) 180+/-45 to 162+/-
30 x 10(9) l(-1) (P=0.01; n=14), without significantly lowering counts with
EDTA-anticoagulation, consistent with increased platelet aggregation. Hiru
din and EDTA provided stable platelet counts, suggesting that fixation is u
necessary.