Hypoxia-induced pulmonary vascular constriction and arterial elastance is less pronounced in Mpo–/– as compared with WT mice, whereas vascular muscularization is not affected by myeloperoxidase (MPO). (A) Mice were kept under normoxia (NOX) or hypoxia (10% O2, HOX) for 7 days, and the Rho-kinase inhibitor Y27632 was administered i.p. 1 hour prior to sacrifice. Constriction of isolated pulmonary artery segments in response to increasing concentrations of prostaglandin F2α (PGF2α) was assessed by isometric force measurements. n = 5 (WT NOX), 6 (WT HOX), 4 (WT HOX Y27632), 5 (Mpo–/– NOX), 7 (Mpo–/– HOX), 6 (Mpo–/– HOX Y27632); *P < 0.05 vs. WT HOX, §P < 0.01 vs. WT HOX, #P < 0.001 vs. WT HOX. Data represent mean ± SEM. (B) Effective arterial elastance (Ea) of WT and Mpo–/– mice after 28 days of NOX or HOX was calculated from right ventricular pressure-volume analyses. n = 3 (WT, Mpo–/– NOX), 8 (WT HOX), 9 (Mpo–/– HOX); *P < 0.05, **P < 0.01. (C) Percentages of nonmuscularized, partially muscularized, and fully muscularized pulmonary arteries of diameters of 20–70 μm and 70–150 μm were assessed in immunohistochemically stained lung sections from mice after 28 days of NOX and HOX. n = 4 (WT NOX), 5 (Mpo–/– NOX), 12 (WT HOX), 14 (Mpo–/– HOX); *P < 0.05, **P < 0.01, ***P < 0.001. (D) Representative images of lung sections: brown, von Willebrand factor; dark blue, α-smooth muscle actin. Scale bar: 20 μm. Data in B and C represent median with interquartile range; whiskers indicate minimum to maximum. Statistical analysis was performed for A with 1-way ANOVA for repeated measures and, for B and C, with 1-way ANOVA followed by LSD post hoc test.