Inhibition of Murine Pulmonary Microvascular Endothelial Cell Apoptosis Promotes Recovery of Barrier Function under Septic Conditions

Figure 5

Caspase activity contributes to persistent septic PMVEC macromolecular hyperpermeability. (a) Inhibition of caspase activity (Z-VAD, 100 μM; Q-VD, 50 μM) following cytomix stimulation did not appear to affect mouse PMVEC TEER at any of the time points examined versus vehicle treatment (dimethyl sulfoxide [DMSO]). In contrast, septic increases in macromolecular flux across PMVEC, including EB-albumin (b) and FITC-dextran (c), were significantly attenuated at 16 h and 24 h after cytomix by inhibition of caspase activity. Dashed lines indicate average basal level (treated with vehicle alone). Of note, inhibition of caspase activity had no effect on septic PMVEC increases in macromolecular flux at earlier time points (4 h and 8 h). and represent and 0.01 compared with PBS, respectively (two-way ANOVA). = 6–8.

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