The liberation of vascactive substances, kinins, from plasma kininogen (HMWK) by plasma kallikrein is implicated in the pathogenesis of bacterial shock. This proces is initiated by the reciprocal activation of Hageman Factor (FXII) and prekallikrein (PK) which may occur during sepsis by the actions of bacterial cell fragments. Of 9 patients with bacterial shock clinical and laboratory data were collected simultaneously at intervals of at least 4 hours, and averaged per patient. Bacteria were recovered from the site of infection of all patients and on culture of blood from 8 patients and involved both Gram-negative (n=7) as- well as Gram-positive (n=2) organisms. Circulatory shock was documented by clinical signs, oliguria, hypotension and blood lactate elevations above 2 mM/L. Mean Arterial Pressure was 79 + l9(SD)mmHg and Lactate 7.0±3.7 mM/l. FXII, FXI, PK and HMWK were measured functionally by clotting assay (c) and/or quantitatively by rocket immuno-electro- phoresis (ag) and expressed as percentage of a normal plasma pool of 40 donors (mean ± SD): These data support the theory of the extensive involvement of this system in the pathogenesis of bacterial shock, since the very low values measured indicate excessive consumption of these factors. Moreover, the 3 patients who died during shock had significantly lower values for FXII- antigen than the 6 patients who recovered from shock (36±13 vs 52±4, p<0.001), in concert with the hypothesis that a more serious invasion with bacteria causes a greater activation of FXII and thus a more severe clinical picture. To this extent these results are at variance with previous reports.