Abstract 850: Dietary Nitrite Supplementation Protects Against Myocardial Ischemia-Reperfusion Injury by Increasing Myocardial Nitric Oxide Stores
Background: Nitrite has long been considered to be an inert oxidative metabolite of nitric oxide (NO). However, recent work has demonstrated that nitrite represents a major tissue storage form of NO that is reduced to NO during ischemic or hypoxic events. Previous studies have shown that an acute administration of nitrite protects against myocardial ischemia-reperfusion (MI-R) injury. However, the contribution of dietary nitrite in maintaining tissue stores of nitrite, NO homeostasis, and MI-R injury is not known. We, therefore, investigated dietary nitrite supplementation and insufficiency in mice and the effects of this manipulation on blood and myocardial NO levels and response to MI-R injury.
Methods and Results: Mice fed a standard diet with supplementation of dietary nitrite (50 mg/L) in their drinking water for 7 days exhibited significantly higher plasma and myocardial levels of nitrite and nitroso (RXNO, marker of NO) and displayed a 48% reduction in infarct size following MI-R. Conversely, mice fed a low NOx diet for 7 days exhibited significantly diminished plasma and myocardial levels of nitrite and RXNO and a 28% increase in infarct size following MI-R. Supplementation of nitrite in the drinking water for 7 days reversed the effects of the low NOx diet.
Conclusions: These data demonstrate the influence of dietary nitrite intake on plasma and myocardial levels of nitrite and NO and illustrates the cytoprotective effects of dietary nitrite supplementation and consequences of nitrite deficiency on the pathophysiology of MI-R injury. Furthermore, these data suggest that dietary nitrite may represent a novel means by which to attenuate MI-R injury.