Anne-Marie Koop

30 the rats (ABCDE-system), as reported previously. 6,18 We further aimed to relate the presence of clinical symptoms of RVF to specific hemodynamic, pathophysiologic and molecular patterns of RV function, using echocardiography, pressure-volume analysis and transcriptome-wide expression profiling in the RV. While a number of previous studies have compared different phenotypes, these were generally induced by different stressors (e.g. Sugen + hypoxia vs. PAB or monocrotaline vs. PAB or Sugen+hypoxia). Such comparisons are very interesting and have yielded considerable insight in the divergent responses of the RV to different physiological and chemical stressors. However, it remains unclear whether the differences found in these studies represent different stages of RVF or merely reflect the different stressors used. We aimed to solve this problem. To this end we compared two groups of rats that all underwent the same PAB banding, but either had or had not developed clinical symptoms of RVF.