Heparinisation, platelet activation and cardiopulmonary bypass
EW Muriithi, EM Milne, #P Wanikiat, #RA Armstrong, DJ Wheatley, PR Belcher
University of Glasgow Dept. of Cardiac Surgery, & #Queen Margaret College, Edinburgh.
Objective: Cardiopulmonary bypass (CPB) is associated both with neutrophil activation and failure of platelets to form large stable aggregates1. We aimed to determine the hitherto unknown effect of neutrophil activation on platelet aggregation in whole blood.
Methods: 14 patients of median age [interquartile range] 61[53-64] years, undergoing routine aorta-coronary bypass grafting and NSAID-free for over 7 days, were studied before and after heparin, and at end-CPB. Whole blood, anticoagulated with rHirudin to maintain normocalcaemia, was stirred to induce spontaneous platelet aggregation, before agonist addition. Macroaggregatory response to collagen (0.6mg.ml-1) or the neutrophil stimulant fMLP (10-7M) was determined by whole blood impedance aggregometry. Microaggregation was measured by counting unaggregated single platelets (corrected for haemodilution).
Results: Before CPB, heparin significantly reduced the platelet count from 127 x109L-1 [110-170] to 95 x109L-1 [64-117] (p=0.023). Heparin reduced collagen-induced macroaggregation from 14.4 cm [12.1-17.0] to 1.3 cm [0.3-5.6] (p<0.0001). CPB had no additional effect. At each stage, collagen-induced microaggregation was well preserved1. Ex vivo fMLP caused platelet macroaggregation(p<0.0001) which was abolished by heparin, and microaggregation (p=0.0001), which was not inhibited by heparin.
Conclusions:
Reference: 1Menys VC et al. Thromb Haemost 1994;72:511-18
