offline over 8-10 beats, sampled within 1 minute of CO measurement. From these tracings, RV (RVSP) and PA (PASP) systolic pressures were measured. Pulmonic valve peak (PG) and mean (MG) gradients were also measured, as was mean right atrial pressure (RAP). Valve flow was calculated and the pulmonic valve orifice area was estimated by the Gorlin formula. The systolic tricuspid valve gradient (TG) was calculated as [RVSP e RAP]. RESULTS: No significant pulmonic valve gradients were observed at rest, and calculated valve area was 3.61.0 cm2. Both RVSP and PASP increased from semi-upright rest to light exercise, although the increase in RVSP was proportionately greater, and pulmonic valve gradients increased (Table 1). RVSP trended modestly upward with moderate exercise, but PASP did not, and so pulmonic valve gradients trended toward increase further at moderate exercise. The TG increased in keeping with RVSP, and so did not track the stability of PASP from light to moderate exercise (Figure 1). CONCLUSION: In healthy adults without pulmonic stenosis, RVSP and PASP dissociate during exercise stress. During moderate intensity exercise, the peak-to-peak RV-PA gradient exceeded 17 mmHg in over half of cases. This observation suggests that sonographic estimation based on the tricuspid regurgitation jet velocity may overestimate PASP as flow in- creases during exercise. Ontario Graduate Scholarship 271 INHIBITION OF FATTY ACID OXIDATION IS ASSOCIATED WITH IMPROVED RIGHT VENTRICULAR FUNCTION AND METABOLISM IN TWO RAT MODELS OF PULMONARY ARTERIAL HYPERTENSION A Ahmadi, J Renaud, J Petryk, T Hadizad, T Ruddy, J Dyck, R Beanlands, R deKemp, G Lopaschuk, L Mielniczuk Ottawa, Ontario BACKGROUND: Pulmonary arterial hypertension (PAH) leads to right ventricular (RV) failure that is associated with inef- ficient myocardial oxidative metabolism. We hypothesized that a pharmacologic inhibition of fatty acid oxidation im- proves overall oxidative metabolism and function in PAH rats. METHODS: Two PAH models were generated in male Sprague Dawley rats: Sugen_Hypoxia (SugHx) and pulmonary artery banding (PAB). A malonyl CoA decarboxylase inhibitor (MCDI), an inhibitor of fatty acid transfer into the mito- chondria, was given orally (100 mg/kg/day) for 3wks after PAH induction. The controls received the drug vehicle. PAB rats had sham controls for MCDI and vehicle groups. Millar catheterization for RV systolic pressure (RVSP), single-photon emission computed tomography (SPECT) for RV ejection fraction (RVEF) and positron emission tomography (PET) for metabolism were performed. PET tracers were a glucose analogue ([18F]fluoro-2-deoxy-glucose (FDG)), a fatty acid (14(R,S)-[18F]fluoro-6-thia-hepadecanoic acid (FTHA)) and [11C]-acetate that reflected glucose standard uptake values (SUVs), fatty acid SUVs and total RV oxidative activity, respectively. [11C]-acetate is cleared from the tissue by mitochondrial oxidation and its value was reported as 1/min. RESULTS: RVSP decreased in SugHx rats treated with MCDI compared to vehicle (65.33.4 vs 114.45.7mmHg; p < 0.001) whereas it did not differ with MCDI treatment in PAB rats. RVEF was equivalent in SugHx and PAB rats treated with vehicle. RVEF improved in MCDI-treated SugHx rats (67.61.9 vs 60.07.2%; p¼0.06) as well as MCDI-treated PAB rats (70.60.9 vs 64.00.6%; p¼0.003). The RVEF difference between MCDI-treated rats from the two models was not significant (p¼0.34). MCDI treatment also did not change RVEF in sham rats (80.02.0 vs 78.70.4). MCDI treatment reduced FTHA SUVs in SugHx (2.00.4 vs 4.20.8; p¼0.008) and PAB (1.80.2 vs 5.81.0; p¼0.05) rats. In the sham groups, MCDI did not change FTHA SUVs. MCDI treatment was not associated with FDG SUV changes in either PAH model. However, PAB rats (MCDI and vehicle) had 8517% higher FDG SUVs than their sham controls (p < 0.001). MCDI treatment increased 11C-acetate clearance in SugHx (0.1900.020 vs 0.0660.004 1/min; p < 0.001) and in PAB (0.1360.003 vs 0.0490.002 1/min; p < 0.001) rats. CONCLUSION: The two PAH models were comparable in terms of RV function and showed equal RVEF improvements with MCDI treatment. This was associated with reduced RV fatty acid metabolism and increased overall oxidative rates. The Abstracts S167