Reduction of heparin binding to and inhibition of platelets by aprotinin.
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 heparin-induced 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 to platelets.
John
L C
LC
Department of Cardiothoracic Surgery, St. Bartholomew's Hospital, London, England.
Rees
G M
GM
Kovacs
I B
IB
D000244:Adenosine Diphosphate / Q000494:pharmacology; D007611:Aprotinin / Q000494:pharmacology*; D001777:Blood Coagulation / Q000187:drug effects; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D006487:Hemostasis / Q000187:drug effects; D006493:Heparin / Q000378:metabolism / Q000494:pharmacology*; D006494:Heparin Antagonists / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000187:drug effects; D010976:Platelet Count; D013997:Time Factors; D014316:Tritium
D006494:Heparin Antagonists; D014316:Tritium; D000244:Adenosine Diphosphate; D006493:Heparin; D007611:Aprotinin