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Updated: Aug 6, 2026

Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro
Published on: March 19, 2016
Autologous blood transfusion for cardiopulmonary bypass: effects of storage conditions on platelet function
Ian R Ramnarine1, Michael J Higgins, Anne McGarrity
1Department of Cardiac Surgery, Glasgow Royal Infirmary, Glasgow, United Kingdom.
Objectives:
Cardiopulmonary bypass impairs formation of large stable platelet aggregates (macroaggregation), although formation of small aggregates (microaggregation) is preserved. A factor in the uncertain benefits of intraoperative autologous blood transfusion may be the effects of storage on platelet function. The effects of citrate preservative and heparinization before storage on platelet function was therefore assessed.
Methods:
Twenty-seven patients undergoing elective coronary artery bypass grafting were randomly allocated to have 450 to 1,000 mL of blood taken into CPDA anticoagulant bags either before (n = 14) or after heparinization (n = 13). Samples from the patients and stored blood were anticoagulated with rhirudin, 200 U/mL. The macroaggregatory response to submaximal collagen was measured by impedance aggregometry and microaggregation by single platelet counting.
Results:
During macroaggregation, before cardiopulmonary bypass, the ex vivo median (interquartile range) response was 16.3 (12.4-18.7) Omega. This decreased 10 minutes after heparin to 8.9 (3.3-11.0) Omega (p < 0.0001). In the blood bags (in vitro), the initial response for nonheparinized blood was 4.8 (0.1-7.5) Omega (p < 0.002 v ex vivo) and at end-cardiopulmonary bypass was 2.4 (1.6-8.2) Omega. During microaggregation, in vivo heparinization decreased microaggregation both ex vivo and in vitro in CPDA blood; the in vitro response of nonheparinized blood at end-cardiopulmonary bypass was greater than that seen after in vivo heparinization (p < 0.007). No difference in bleeding or transfusion requirements was seen.
Conclusions:
Collecting blood into CPDA anticoagulant caused a marked deterioration in platelet function. This was worse after in vivo heparinization and included depression of microaggregation.
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