RESUMO
The discrepancies between kininogenase, BAEE-esterase and BAPNA-amidase activity in plasma kallikrein were shown in experiments in vitro. The same discrepancies were detected during examination of children aged under 3 years suffering from bronchopulmonary diseases (acute and lingering pneumonia, bronchial asthma). In these children, prekallikrein, kallikrein and kallikrein inhibitor were determined at a time by the 3 methods (esterase, test-tube chromatographic and kininogenase ones). It has been shown that the kininogenesis intensity could be assessed objectively only in the measurement of the kininogenase activity of kallikrein contained by the whole plasma or its fractions. The esterase technique characterizes total factors of contact activation and does not reflect the activity of kallikrein, prekallikrein and kallikrein inhibitor. The test-tube chromatographic method might be regarded as objective only in the measurement of the kininogenase activity of the fractions that contain kallikrein or prekallikrein.
Assuntos
Asma/sangue , Calicreínas/sangue , Pneumonia/sangue , Pré-Escolar , Humanos , Calicreínas/antagonistas & inibidores , Métodos , Pré-Calicreína/análiseRESUMO
It is suggested that the kininogenesis should be assessed from 3 forms of kallikrein which are detected on the basis of their kininogenase activity in whole blood plasma. Heating of blood plasma acidified to pH 3.0 for 15-20 min at 61 degrees C allows for the conditions under which the kallikrein inhibitors (alpha 1-antitrypsin, alpha 2-macroglobulin) are destroyed whereas kallikrein, prekallikrein, low- and high-molecular kininogens (HMK) are preserved, thus constituting a complex of proteins making the kininogenase reaction feasible. Addition of purified preparations of HMK to the neutralized samples of normal and sick individuals' plasma permitted the demonstration that as the kallikrein is raised, the kininogenesis gets actually activated, during which the blood manifests, in the presence of kallikrein hyperactivity, a sufficient amount of HMK. Provided the kallikrein content drops by 50%, the kininogenesis is reduced, which is accounted for by depletion of blood HMK. A 70%- and a greater decrease in the kallikrein content attests to the kininogenesis reduction because of the diminished levels of HMK, prekallikrein and kallikrein. The regularities described have been confirmed by the agreement between the blood plasma kallikrein level and the concentration of blood free kinins revealed during examination of 68 normal individuals and 231 patients suffering from different inflammatory-allergic diseases of the respiratory and hepatobiliary organs, and from diabetes mellitus.