Figure 3.

Time course of hypoxic right ventricular hypertrophy: protection by HO-1 overexpression. (a) Non-Tg mice were exposed to hypoxia (8–10% O₂) for 18 h, 5 days (d), or 2–3 weeks (w). Development of RVH after hypoxic exposure was determined by the RV/(LV + S) ratio as described in Materials and Methods. *, P < 0.01, **, P < 0.001 vs. time point 0 (n = 6 for each group, one-way ANOVA). (b) Tg homozygous, heterozygous, and non-Tg control mice from founder 1 and homozygous Tg and non-Tg mice from line 2 were exposed to normoxia or hypoxia for 3 weeks. Under normoxia, line 1 homozygous Tg (n = 19), heterozygous Tg (n = 6), and non-Tg controls (n = 14) as well as line 2 homozygous Tg (n = 5) or non-Tg (n = 5) did not differ in baseline RV/(LV + S) (P > 0.05). After hypoxic exposure, line 1 homozygous Tg (n = 26) and heterozygous Tg mice (n = 8) show significant reduction in RV/(LV + S) as compared with non-Tg controls (n = 22). Similarly, homozygous line 2 Tg mice (n = 5) manifest significantly lower RV/(LV + S) values as compared with their non-Tg controls (n = 5) exposed to hypoxia. (*, P < 0.05, **, P < 0.005 vs. hypoxic controls; †P < 0.01 vs. normoxic controls, Mann–Whitney U test). Data are mean ± SEM.