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Different activation patterns in the plasma kallikrein‐kinin and complement systems during coronary bypass surgery
Author(s) -
Kongsgaard U. E.,
SmithErichsen N.,
Geiran O.,
Amundsen E.,
Mollnes T. E.,
Garred R
Publication year - 1989
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1989.tb02921.x
Subject(s) - cardiopulmonary bypass , prekallikrein , medicine , kallikrein , complement system , anesthesia , heparin , bypass surgery , kinin , cardiology , bradykinin , immunology , artery , antibody , receptor , biochemistry , biology , enzyme
Components of the plasma kallikrein‐kinin and complement systems were determined in patients undergoing open heart surgery with cardiopulmonary bypass. Spontaneous kallikrein activity (KK), plasma prekallikrein (PKK), functional kallikrein inhibition capacity (KKI), C3 activation products (C3‐act), and the terminal complement complex (TCC) were measured. A marked, transitory increase in KK and a decrease in PKK were found prior to cardiopulmonary bypass just after heparin injection. An additional decline in PKK and KKI during bypass with a return to near control levels in the postoperative period was observed. C3‐act increased in all patients during bypass, reaching a peak value at wound closure. The TCC concentration also increased significantly during cardiopulmonary bypass, returned to control levels in the early postoperative period, and then increased again in the late postoperative period. It is concluded that activation of the kallikrein‐kinin system started after injection of heparin, prior to cardiopulmonary bypass. Activation of both the initial and the terminal complement cascade, however, started only after onset of cardiopulmonary bypass.