Table 1.
Pleural Fluids at 24 h |
|||||
---|---|---|---|---|---|
scuPA Treatment, mg/kg | Adjunct | Adjunct Dose, mg/kg | Outcome (GLIS)* | PAI-1, nM† | αM/uPA, nM |
0.25 | Mouse IgG | 0.5 | 17 | 2.4 ± 0.6 | 0.45 ± 0.08 |
0.25 | MA-33B8 | 0.5 | 3 | 2.1 ± 0.4 | 1.6 ± 0.6 |
0.25 | MA-56A7C10 | 0.5 | 50 | 6.7 ± 0.9 | 0.34 ± 0.07 |
0 | Mouse IgG | 0.5 | 50 | 3.2 ± 0.4 | <0.02 |
Levels of active PAI-1 and αM/uPA complexes are means ± SE; n = 2 for each group. IPFT, intrapleural fibrinolytic therapy; scuPA, prourokinase; αM, α-macroglobulin; uPA, urokinase.
Gross lung injury score (GLIS; 25, 48) was determined by counting number of strands, webs, and aggregates of intrapleural fibrin organizations to quantify the extent of the injury. GLIS from 0 to 10 and from 11 to 50 correspond to successful or unsuccessful IPFT, respectively. The differences in median values among the treatment groups were statistically significant (P = 0.025).
Plasminogen activator inhibitor-1 (PAI-1) activity was estimated from the results of inhibition of exogenous two-chain uPA (tcuPA; 0.5 nM), added to the samples of pleural fluids as previously described.