Abstract 17524: Nitrite Decreases Oxidative Stress Through Inhibition of Nuclear Factor-kappaB (NF-κB) Signaling Pathway During Chronic Ischemic-Induced Heart Failure

Background: Nitric oxide (NO) bioavailability is reduced in the setting of congestive heart failure (HF). We have previously reported that sodium nitrite (NaNO2) ameliorates acute myocardial ischemia-reperfusion (MI-R) when administered at reperfusion. NF-κB mediates cellular oxidative stress and its activation increases the severity of myocardial hypertrophy and heart failure (HF). However, no evidence exists as to whether increasing NO bioavailability via NaNO2- therapy attenuates chronic HF following acute myocardial infarction via inhibition of NF-κB activation. Methods: Male C57/BL6J mice (n=13-15/group) underwent 60 min. of MI induced by LCA occlusion followed by 4 weeks of reperfusion. NaNO2 or saline vehicle (VEH) was administered at a dose of 165 μg/kg (intra cardiac injection) at reperfusion and then daily for 4 weeks in the drinking water (100 mg/L). Left ventricular ejection fraction (LVEF) was determined at baseline and at 4 weeks of reperfusion using high frequency ultrasound. At 4 weeks of ...