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*Department of General Anesthesiology and Intensive Care B, University of Vienna, School of Medicine, Vienna, Austria;
Department of Pathology,
Artificial Heart Laboratory, and
§Division of Nephrology & Hypertension, Department of Medicine, University of Utah School of Medicine; and
||Research and
¶Medical Services, Veterans Affairs Medical Center, Salt Lake City, Utah
Address correspondence and reprint requests to Sibylle A. Kozek-Langenecker, MD, Department of Anesthesiology and General Intensive Care, University of Vienna, Währinger Gürtel 18-20, 1090-Vienna, Austria. Address e-mail to sibylle.kozek-langenecker{at}univie.ac.at
The effects of heparinization and the reversal of heparin activity on platelet function after cardiopulmonary bypass have not been well defined. Flow cytometry has become a convenient and powerful technique for characterizing platelets. We examined the expression of a secretion marker (P-selectin) and an aggregation marker (activated fibrinogen receptor GP IIb-IIIa) on normal platelets in response to heparin, heparinase 1, and protamine in vitro using whole blood flow cytometry. Unfractionated heparin increased adenosine diphosphate-induced expression of P-selectin and GP IIb-IIIa in a dose-dependent manner. Heparinase 1 alone decreased both markers of platelet activation. Protamine alone increased P-selectin expression but had no effect on GP IIb-IIIa expression. Heparinase 1 antagonized the stimulatory effect of heparin on both markers. In contrast, protamine antagonized the effect of heparin on GP IIb-IIIa expression but potentiated the effect of heparin on P-selectin expression. These in vitro observations suggest that 1) both heparin and its reversal agents affect platelet secretion and aggregation, and 2) heparinase 1 reverses heparin-induced platelet preactivation more effectively than protamine.
Implications: This experimental in vitro study demonstrates that heparin and its reversal agents affect platelet secretion and aggregation.
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