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The Annals of Thoracic Surgery, Vol 55, 1033-1041, Copyright © 1993 by The Society of Thoracic Surgeons
S Westaby
Aprotinin is a nonspecific serine protease inhibitor extracted from bovine
lung. It was first used during cardiopulmonary bypass to inhibit
plasmin-induced complement activation. By chance significant reductions of
blood loss and blood requirements were noted in treated patients.
Subsequent investigation showed improved hemostasis to result from
protection of platelet adhesive receptors (Gp Ib) at the onset of
cardiopulmonary bypass. Without aprotinin the contact system of plasma is
massively activated on first passage through the cardiopulmonary bypass
circuit. Activation of the intrinsic coagulation pathway causes thrombin
formation, which impairs platelet adhesive function. Aprotinin blocks
contact activation of the kallikrein system during cardiopulmonary bypass
and in synergy with heparin prevents thrombin formation through inhibition
of the intrinsic clotting cascade. It is likely that neither thrombin nor
platelets become involved in the blood- foreign surface contact activation
process in aprotinin-treated patients. The fact that the hemostatic process
is affected from the very beginning of cardiopulmonary bypass is
substantiated by the fact that low-dose aprotinin therapy (2 x 10(6) KIU
aprotinin added to the pump prime) leads to the same preservative effect on
Gp Ib receptors and blood loss as continuous high-dose infusion (6 x 10(6)
KIU) throughout the whole surgical procedure. In the presence of heparin
aprotinin prolongs the activated clotting time and the in vitro activated
partial thromboplastin time. This has important implications for heparin
dosage. An inhibitory effect on the endothelial cell anticoagulant function
may also have consequences during hypothermic low flow and circulatory
arrest states.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Aprotinin in perspective
Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, England.
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