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. 2017 Aug 31;314(1):L54–L68. doi: 10.1152/ajplung.00579.2016

Table 1.

Effects of MA-33B8 and MA-56A7C10 on the outcome of IPFT with 0.25 mg/kg scuPA and on the levels of active PAI-1 and αM/uPA complexes in the pleural fluids at 24 h after IPFT

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.