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Ann Thorac Surg 1999;67:79-84
© 1999 The Society of Thoracic Surgeons


Original Articles

Platelet aggregation during cardiopulmonary bypass evaluated by a laser light-scattering method

Koji Kawahito, MDa, Eiji Kobayashi, MDb, Hideaki Iwasa, MDc, Yoshio Misawa, MDa, Katsuo Fuse, MDa

a Department of Cardiovascular Surgery, Jichi Medical School, Tochigi, Japan
b Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan
c Omiya Medical Center, Jichi Medical School, Saitama, Japan

Accepted for publication June 16, 1998.

Address reprint requests to Dr Kawahito, Department of Cardiovascular Surgery, Jichi Medical School, Yakushiji, Minami-Kawachi, Kawachi, Tochigi 329-04, Japan
e-mail: bza06625{at}niftyserve.or.jp

Background. In regard to postoperative bleeding, the most important consequence of cardiopulmonary bypass (CPB) is the loss of aggregability. However, the mechanism of platelet aggregation loss during CPB is unclear. Newly developed particle-counting methods that use light scattering can be used to quantify changes in the number of platelet aggregates of different sizes after application of an aggregating stimulus. Using a light-scattering method, we investigated changes in platelet aggregation during cardiac operation.

Methods. Nineteen patients undergoing CPB were evaluated. Blood samples were obtained before the operation, 1 hour after initiation of CPB, at the end of CPB, at the end of the operation, and on day 1 after the operation. Platelet aggregation after stimulation by 2.5 µmol/L adenosine diphosphate and 2.0 µg/mL collagen was determined; small (9 to 25 µm), medium (25 to 50 µm), and large (50 to 70 µm) aggregates were counted.

Results. Generation of medium and large aggregates after stimulation with adenosine diphosphate and collagen were significantly decreased with CPB, whereas, in spite of hemodilution, the quantity of the small aggregates was maintained at the elevated level.

Conclusions. These results reflect the fact that CPB does not affect the first phase of aggregation. It suggests that platelet dysfunction associated with CPB is mainly caused by an inhibition in the development of small aggregates into larger aggregates.




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