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Formation of C1s-C1-inhibitor, kallikrein-C1-inhibitor, and plasmin- alpha
2-plasmin-inhibitor complexes during cardiopulmonary bypass
YT Wachtfogel, PC Harpel, LH Edmunds and RW Colman
Thrombosis Research Center, Temple University School of Medicine,
Philadelphia, PA 19140.
Stimulation of platelets and neutrophils occurs during clinical
cardiopulmonary bypass. We investigated whether the classical complement,
contact, or fibrinolytic pathways are activated as potential sources of
neutrophil agonists. Using enzyme-linked immunosorbent "sandwich" assays
specific for C1s-C1-and kallikrein-C1- inhibitor complexes respectively, we
found that there was a modest increase in plasma levels of each complex
after clinical cardiopulmonary bypass was completed. The increased
concentration of enzyme-inhibitor complexes reverted to baseline within 24
hours. Since these complexes are cleared in vivo, we measured their
formation by assaying their plasma levels during in vitro simulated
extracorporeal circulation. Over a period of two hours, C1s-C1-inhibitor
complexes rose from a baseline of 2 +/- 1 nmol/L to 21 +/- 2 nmol/L, and
kallikrein-C1-inhibitor complexes rose from 2 +/- 1 nmol/L to 25 +/- 5
nmol/L. However, there was no evidence of either in vivo or in vitro
plasmin-alpha 2-plasmin-inhibitor complex formation. These results indicate
that the pathways of classical complement and contact activation, but
probably not fibrinolysis, may be associated with neutrophil activation
seen during clinical cardiopulmonary bypass.
Volume 73,
Issue 2,
pp. 468-471,
02/01/1989
Copyright © 1989 by The American Society of Hematology
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