Assay of kallikrein inhibitors and levels of acetone-activated kallikrein in plasma specimens from reactors to dextran or to contrast media.

The average level of kallikrein assayed as acetone-activated plasminogen activator (PGA) in plasma specimens from 10 reactors to clinical dextran or to radiographic contrast media did not differ from the level in 16 controls. This result was obtained in plasminogen-free citrated plasma stabilized with benzamidine. In the absence of benzamidine a significant reduction of PGA activity was registered in the reactor plasma, but not of activity against the tripeptide substrate S-2302 or the ester substrate BAEe. After storage of the plasma specimens for 12 to 18 months at -70 degrees, the PGA activity obtainable in reactor plasma had increased to the level registered in control plasma. Known inhibitors of plasma kallikrein and of histidine-rich glycoprotein (HRG) were assayed by radial immunodiffusion. The levels of alpha 2-macroglobulin, antithrombin-III and HRG were within the normal range in plasma from reactors, the level of C1-esterase inhibitor was slightly increased (116%), and the level of alpha 1-antitrypsin was higher than normal (124%). Evidence is provided that the loss of PGA activity taking place during acetone activation of fresh reactor plasma could not be due to a transition of native alpha-kallikrein to 3-chain beta-kallikrein. It is concluded that a plasma constituent unstable during storage is responsible for the selective and partial loss of PGA activity registered in reactor plasma.