Abstract 046: Cardiac Mitochondria are Impaired After Transient Neonatal High Oxygen Exposure in a Rat Model of Prematurity-Related Condition

• DOI: 10.1161/hyp.72.suppl_1.046
• Publication Date: 2018-12-06T15:08:55Z
• Authors: Daniela Ravizzoni...; Ying He; Muhammad Oneeb Re...; Alyson Deprez; Camille Girard-Bock; Anik Cloutier; Gael Cagnone; Perrine Gaub; Jean-Sebastien Joyal; Thuy Mai Luu; Anne Monique Nuyt
• Keywords: 03 medical and health sciences; 0302 clinical medicine; 3. Good health

The heart relies on adequate mitochondrial (mito) ATP production to match myocardial demand, mostly through oxidative phosphorylation. Preterm birth (PT) results in ex utero development of an immature myocardium and PT-born individuals represent a newly recognized group at high risk cardiovascular diseases. Our has shown that newborn rats exposed oxygen (O 2 ), mimicking PT-related conditions, develop O -induced cardiomyopathy (OIC) dysfunction later life. However, whether mito impairments prevail the programmed left ventricle (LV) changes associated with PT is unknown. We aimed determine OIC altered LV characteristics 4 wks-old rats. Male rat pups were kept their mother 80% or room air (Ctrl) from days 3 10 Results are mean±SEM; vs. Ctrl compared using t-test (n=4/group.P<0.05). At wks, extracellular flux analysis isolated cardiomyocytes revealed significantly decreased consumption rate (12.14±5.74 67.39±13.61 pmoles/min/ug). show reduced copy number determined by ratio between genomic DNA (26.7±6.30 52.7±7.32), biogenesis markers Pgc1α (0.59±0.14 1.18±0.25), citrate synthase (0.20±0.16 1.60±0.56) mRNA, Complex IV (0.66±0.15 1.26±0.09) protein expression. Gene expression (RT-PCR) key glycolytic enzymes, hexokinase (3.34±0.59 0.88±0.39) glucose-6-phosphate dehydrogenase (2.85±0.48 0.58±0.08) increased, indicating shift toward glycolysis. also found have higher mtROS (7581±51 5191±99, fluorescence arbitrary units) antioxidant SOD2 (0.84±0.09 1.04±0.05). Taken together our indicate neonatal hyperoxia exposure leads function impaired phosphorylation capacity juvenile animals. Further studies needed role long-term increased susceptibility failure observed after deleterious conditions.