Activation of the kallikrein-kinin system by cardiopulmonary bypass in humans

We used cardiopulmonary bypass (CPB) as a model of activation of the contac t system and investigated the involvement of the plasma and tissue kallikre in-kinin systems (KKS) in this process. Circulating levels of bradykinin an d kallidin and their metabolites, plasma and tissue kallikrein, low and hig h molecular weight kininogen, and kallistatin were measured before, during, and 1, 4, and 10 h after CPB in subjects undergoing cardiac surgery. Brady kinin peptide levels increased 10- to 20-fold during the first 10 min, retu rned toward basal levels by 70 min of CPB, and remained 1.2- to 2.5-fold el evated after CPB. Kallidin peptide levels showed little change during CPB, but they were elevated 1.7- to 5.2-fold after CPB. There were reductions of 80 and 60% in plasma and tissue kallikrein levels, respectively, during th e first minute of CPB. Kininogen and kallistatin levels were unchanged. Ang iotensin-converting enzyme inhibition did not amplify the increase in brady kinin levels during CPB. Aprotinin administration prevented activation of t he KKS. The changes in circulating kinin and kallikrein levels indicate act ivation of both the plasma and tissue KKS during activation of the contact system by CPB.