Three weeks after PAB, placebo-treated mice showed several signs of RV dysfunction as compared to sham-operated mice. PAB led to RV systolic dysfunction, as indicated by an increase in end-systolic volume (17.3±1.0 ml vs. 29.2±2.5 ml [Sham vs. PAB]), decreased RV stroke volume (40.5±2.3 ml vs. 23.0±3.3 ml) and decreased RV ejection fraction (70.0±1.0 % vs. 43.0±3.5 %). Treatment with sildenafil did neither lead to significant changes in RV end-systolic volume, RV stroke volume nor RV ejection fraction, whilst treatment with BAY 41-8543 and combination treatment led to significant improvements. (RV end-systolic volume: 29.2±2.5 vs. 23.6±3.3 vs. 24.6±1.1 vs. 19.1±3.8; RV stroke volume: 23.0±3.3 vs. 27.3±2.3 vs. 32.1±3.8 vs. 31.8±1.3; RV ejection fraction: 43.3±3.5 vs. 54.1±3.0 vs. 55.7±3.7 vs. 63.8±4.4 [all values as %; placebo vs. sildenafil vs. BAY 41-8543 vs. combination treatment]). PAB mice showed RV hypertrophy (0.022±0.003g vs. 0.032±0.006g) and an increased RV/(LV-S) ratio (0.25±0.03 vs. 0.39±0.1). Drug treatment had no effects on either RV hypertrophy nor RV/(LV+S) ratio. RV pressure was increased in PAB mice (30.0±3.0 mmHg vs. 50.8±12.2 mmHg) and did not change under drug treatment. Histological assessment of fibrosis showed that the collagen content increased in banded mice, sildenafil had no effects on collagen content, and BAY 41-8543 and combination treatment both decreased the amount of collagen (7.6±2.1 vs. 1.2±0.1 8.8±5.8 vs. 3.3±1.2 vs. 3.3±1.2 [all values as %; placebo vs. sham vs. sildenafil vs. BAY 41-8543 vs. combination treatment]).