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The Annals of Thoracic Surgery, Vol 44, 640-645, Copyright © 1987 by The Society of Thoracic Surgeons
W van Oeveren, NJ Jansen, BP Bidstrup, D Royston, S Westaby, H Neuhof and CR Wildevuur
Cardiopulmonary bypass (CPB) is associated with activation of humoral
systems, which results in the release of proteases. These proteases may
affect platelets and stimulate granulocytes. In the present study, the
protease inhibitor aprotinin was given in high doses to 11 patients to
achieve plasma concentrations of more than 150 kallikrein inactivator units
per milliliter during CPB. At such concentrations, kallikrein and plasmin
are effectively inhibited. This treatment resulted in platelet preservation
during CPB. Platelet numbers were virtually unaffected, and thromboxane
release was prevented in the aprotinin-treated group in contrast to the
control group. Postoperatively, hemostasis was significantly better
preserved after aprotinin treatment (blood loss of 357 ml in the treated
group versus 674 ml in the untreated group; p less than 0.01). Since
tissue-plasminogen activator activity was similar in both groups, the
improved hemostasis most likely should be attributed to platelet
preservation. Furthermore, aprotinin lessened neutrophilic elastase
release, which might contribute to decreased pulmonary dysfunction in
patients at risk.
ARTICLES
Effects of aprotinin on hemostatic mechanisms during cardiopulmonary bypass
Department of Cardiopulmonary Surgery, University Hospital, Groningen, The Netherlands.
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J. H. Levy, R. Pifarre, H. V. Schaff, J. C. Horrow, R. Albus, B. Spiess, T. K. Rosengart, J. Murray, R. E. Clark, P. Smith, et al. A Multicenter, Double-Blind, Placebo-Controlled Trial of Aprotinin for Reducing Blood Loss and the Requirement for Donor-Blood Transfusion in Patients Undergoing Repeat Coronary Artery Bypass Grafting Circulation, October 15, 1995; 92(8): 2236 - 2244. [Abstract] [Full Text] |
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