SummaryIn order to assess the role of the kallikrein-kinin (K-K) system in the pathogenesis of the adult respiratory distress syndrome (ARDS) we have prospectively determined coagulation contact phase, blood gas and hemodynamic parameters in patients with ARDS at 0, 36 and 72 h from diagnosis.Compared to normal values, significantly lower mean levels of factor XII (71.4 ± 9.8%, p <0.0005), prekallikrein (PPK) (52 ± 5.7%, p <0.0005), high molecular weight kininogen (HMWK) (73 ± 2%, p <0.0005) and α2-macroglobulin (α2-M) (51 ± 7.1%, p <0.0005) were found in ARDS patients.The functional kallikrein inhibitory activity (KKI) and Cr esterase inhibitor antigenic (CIINH) were significantly higher in these patients (113.2 ± 5, p <0.005 and 124.7 ± 7.6, p <0.0005 respectively) compared with normal values during the entire study period.The KKI/CIINH ratio decreased significantly in our ARDS patients at 0, 36 and 72 h (p <0.025; p <0.05 and p <0.005 respectively).We found a significant correlation between PPK levels and oxigenation index (r = 0.69, p <0.001), PPK and the static thoracic compliance values (r = 0.64, p <0.001). There was also a significant correlation between PPK levels and Qs/Qt (r = -0.89, p <0.001). ARDS patients that survived presented a stability in the PPK values in successive tests. Nevertheless non-survivors showed a progressive decrease in PPK levels during the follow-up period.Our results suggest that the plasma kallikrein system becomes activated during ARDS and that this activation might increase the lung vessels’ permeability. In addition, PPK levels are in our opinion a useful prognostic parameter in predicting the outcome of ARDS patients.
In order to assess the role of the kallikreinkinin (k-k) system in the pathogenesis of pulmonary oedema, we studied the contact phase factors of blood coagulation, as well as the haemodynamics and blood gas changes in 34 patients with pulmonary oedema, 23 of them with Adult Respiratory Distress Syndrome (ARDS) and 11 with cardiogenic pulmonary oedema (CPO). We have verified significant differences in the haemodynamic pattern and blood gases between the two groups of patients, which corroborate the previously established differences between both types of pulmonary oedema. Our results reveal k-k system activation in ARDS patients, with a significant fall in factor XII (p less than 0.05), prekallikrein (p less than 0.01), alpha-2-macroglobulin (p less than 0.01) and high molecular - weight kininogens (p less than 0.005), with a rise in C1-esterase inhibitor (p less than 0.001) in comparison with patients with CPO. All of the CPO patients had normal prekallikrein levels, whereas 15 out 23 ARDS cases (65%) had decreased prekallikrein values. Our results suggest that the k-k system activation could play a role in the pathogenesis of ARDS. Estimation of prekallikrein levels may be helpful in the differential diagnosis of ARDS.
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