Summary
Alterations of the kallikrein-kinin system consistent with activation and increased
consumption have been re2ported in septic patients and it has been suggested that
this activation could contribute to the development of septic shock.
The aim of this work was to confirm these alterations in septic patients and to investigate
the possible existence of similar changes in subjects developing cardiogenic shock
secondary to myocardial infarction as a model of non septic shock.
Patients with septic shock, especially in fatal cases, showed a highly significant
decrease in levels of factor XII, prekallikrein, high molecular weight kininogen (HMW-kininogen),
α2-macro-globulin (α2-M) and antithrombin III (AT-III). C1-esterase inhibitor (C1-INH) activity was increased
in uncomplicated sepsis but came back to normal or was slightly decreased in septic
shock.
Components and inhibitors of the kallikrein-kinin system were within normal limits
in patients with cardiogenic shock.
Our findings support the idea of a contribution of the kallikrein-kinin system to
the development of septic shock though this system does not seem to play a significant
role in the pathogenesis of cardiogenic shock or seem to be altered as a consequence
of it.
Key words
Factor XII - Kallikrein - Septicemia - Septic shock - Cardiogenic shock