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Ann Thorac Surg 1993;55:1175-1179
© 1993 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery and the Thrombosis Unit, St. Bartholomew's Hospital, London, England
Accepted for publication August 21, 1992.
* Address reprint requests to Dr John, Department of Cardiothoracic Surgery, St. Bartholomew's Hospital, West Smithfield, London EC1A 7BE, England.
The direct effect of aprotinin on in vitro platelet function was assessed by hemostatometry (n = 10). No significant enhancement was demonstrated. However, aprotinin reduced platelet inhibition secondary to heparin. Hemostatometry demonstrated a significant preservation of in vitro platelet function (n = 25) (p = 0.04), which was particularly marked (p = 0.003) in the subgroup (n = 7) demonstrating a severe inhibition of platelet function with heparin. Aprotinin significantly reduced the binding of tritium-labeled heparin to both nonactivated (n = 25) (p = 0.004) and activated platelets (n = 25) (p < 0.0001). We conclude that interference with heparininduced inhibition of platelet function by aprotinin may be one of its hemostatic actions in cardiac surgery. This effect is probably secondary to aprotinin reducing binding of heparin in platelets.
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