Thromb Haemost 1994; 72(04): 511-518
DOI: 10.1055/s-0038-1648905
Original Article
Schattauer GmbH Stuttgart

Macroaggregation of Platelets in Plasma, as Distinct from Microaggregation in Whole Blood (and Plasma), as Determined Using Optical Aggregometry and Platelet Counting respectively, is Specifically Impaired following Cardiopulmonary Bypass in Man

Valentine C Menys
1   The Department of Biological Sciences, The Manchester Metropolitan University, Manchester, London
,
Philip R Belcher
2   Academic Unit of Cardiovascular Medicine, Charing Cross and Westminster Medical School, London
,
Mark I M Noble
2   Academic Unit of Cardiovascular Medicine, Charing Cross and Westminster Medical School, London
,
Rhys D Evans
3   Nuffield Department of Anaesthetics, UK
,
George E Drossos
4   Department of Cardiac Surgery, John Radcliffe Hospital, Oxford, UK
,
Ravi Pillai
4   Department of Cardiac Surgery, John Radcliffe Hospital, Oxford, UK
,
Steve Westaby
4   Department of Cardiac Surgery, John Radcliffe Hospital, Oxford, UK
› Author Affiliations
Further Information

Publication History

Received 20 January 1994

Accepted after resubmission 14 June 1994

Publication Date:
06 July 2018 (online)

Summary

We determined changes in platelet aggregability following cardiopulmonary bypass, using optical aggregometry to assess macroaggregation in platelet-rich plasma (PRP), and platelet counting to assess microaggregation both in whole blood and PRP. Hirudin was used as the anticoagulant to maintain normocalcaemia.

Microaggregation (%, median and interquartile range) in blood stirred with collagen (0.6 µg/ml) was only marginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (92, 96] prebypass; n = 22), whereas macroaggregation (amplitude of response; cm) in PRP stirred with collagen (1.0µg/ml) was markedly impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7,14.3], n = 10; p <0.0001). However, in PRP, despite impairment of macroaggregation (9.1 [8.5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), as in whole blood stirred with collagen. In contrast, in aspirin-treated patients (n = 14), both collagen-induced microaggregation in whole blood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were more markedly impaired, compared with control (both p <0.001).

Similarly, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impaired following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p <0.0002, n = 20), but as found with collagen, despite impairment of macroaggregation (7.2 [3.5,10.9], n = 12), microaggregation was again near-maximal (96 [93,97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelo-fusine) treated patients (5.6 [2.8, 8.6], n = 17; p <0.005 v control), whereas the response to collagen was little different (9.3 v 9.5). In contrast to findings with collagen in aspirin-treated patients, the response to ristocetin was little different to that in controls (8.0 v 8.3). Impairment of macroaggregation with collagen or ristocetin did not correlate with the duration of bypass or the platelet count, indicating that haemodilution is not a contributory factor.

In conclusion: (1) Macroaggregation in PRP, as determined using optical aggregometry, is specifically impaired following bypass, and this probably reflects impairment of the build-up of small aggregates into larger aggregates. (2) Impairment of aggregate growth and consolidation could contribute to the haemostatic defect following cardiac surgery.

 
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