Figure 2.

Nitric oxide regulates functionality of the Ang/TIE signaling axis. (A) Overall survival of CS-challenged mice with or without concurrent administration of the universal NOS inhibitor L-NAME (n = 14 CS, 22 L-NAME mice per group, derived from two independent experiments; p = 0.0013; log rank test). (B) Fold change over control uninfected mice of serum Ang1 and Ang2 levels in CS-challenged mice with or without concurrent administration of L-NAME (paired Wilcoxon rank-sum; n = 4–5 mice per group derived from 3 independent experiments). (C) Accumulation of ROS (O₂⁻) as measured by dihydroethidium staining in the liver of CS-challenged mice with or without concurrent administration of L-NAME as measured by dihydroethidium staining (paired Wilcoxon rank-sum; n = 8 control, 6 CS, 6 L-NAME, all pooled across 3 independent experiments). (D) Overall survival of CS-challenged mice (at LD50) with or without administration of L-NAME 4–6 h prior to challenge (n = 18–21 mice per group, derived from two independent experiments; p < 0.0001; log rank). (E) Survival of CS-challenged mice (at LD90) treated with saline only, L-Arg, Ang1 or combined L-Arg and Ang1 1-h post challenge (n = 15–21 mice per group, derived from two independent experiments; p < 0.0001; log rank test). Boxplots indicate medians with first and third quartiles (25–75%) at the lower and upper bounds of the box; whiskers extend no further than 1.5 × interquartile range from the hinge.