0158 : Benefits of a nutritherapy with glycerophospholipids-DHA versus triglycerides- DHA in preventing pulmonary hypertension and cardiac insufficiency in chronic hypoxemic rats

Background and objectives Chronic hypoxemia induces pulmonary hypertension (PH) leading to cardiac insufficiency, and fish oil (EPA+DHA) seems beneficial to prevent PH. We aimed at investigating the effects of DHA from glycerophospholipids (GPL-DHA) or from algal oil (triglycerides) in preventing experimental PH and heart insufficiency. Procedure The study was conducted in Wistar males rats (n=10 per group) over 7 weeks: a control group (C) in normoxic conditions, two groups maintained in normoxic conditions for 4 weeks and under hypoxic conditions (hypobaric chamber, 0.5 Bar) for the last 3 weeks receiving no DHA (H) or 60-120 mg/kg/ day of DHA as GPL (GPL-D60, GPL-D120) or triglycerides (TG-D120). The thickness of the right ventricle (RV) and the pulmonary artery acceleration time (PAAT) were measured weekly by echocardiography. At the end of the study, pulmonary artery pressure (PAP, invasive catheterization) and the fatty acid profile of lungs and heart were determined. Statistics were done by Mann-Whitney test (p Results Hypoxemia led to i) a high increase of the thickness of the RV and RV hypertrophy, ii) a decrease in PAAT (increase in vascular resistance), ii) a change in DHA level in heart (increase) and in lungs (decrease). The DHA supplementation i) limitated the development of RV dysfunction (–19%/–24% thickness), ii) attenuated the decrease in PAAT (+41% or +76% for GPLDHA60 or 120, +46% for TG-DHA120) and the vascular resistance (–12% PAP), iii) increased DHA level slightly in heart (C: 9.3±2.0a; H: 12.4±3.0b; GPL-D60: 14.2±4.4bc; GPL-D120: 15.6±2.8c; TG-DHA120: 14.3±1.5bc) and highly in lungs (C: 2.1±0.2a; H: 1.9±0.2b; GPL-D60: 2.5±0.4c; GPL-D120: 3.5±0.9d; TG-DHA120: 3.7±0.8d). Conclusions GPL-DHA and TG-DHA partially prevented PH and cardiac remodeling. The effects seem not related only to the total level of DHA in tissues suggesting plausible changes in phospholipid classes. The author hereby declares no conflict of interest