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18th World Congress on Heart Disease



Tadeusz Malinski, Ph.D., Ohio University, Ohio, USA


Background: The functional endothelial cells are the main source of nitric oxide (NO) in the heart. NO release in the beating heart is stimulated by mechanical forces during systole and diastole. NO release can be also stimulated in the heart by chemical pathways, i.e. epinephrine. The highest concentration of NO (1.5 to 2 micromoles/liter) is produced by endocardium. A concentration of peroxynitrite (ONOO-) in the beating heart is minimal (<30 nanomoles/liter). ONOO- is generated after the reaction of NO with superoxide (O2.-). In dysfunctional endothelium, a main source of O2.- is nitric oxide synthase and NAD(P)H.

Methods and Results: Nanosensors with diameter <300 nanometers were used to measure: NO, O2.-, and ONOO-. A module of catheter protected nanosensors was placed in the left ventricular wall of the heart of WKY rats. A rapid increase in NO was observed after 15 s of ischemia. The increase in NO was accompanied by the increase in O2.- and ONOO-. At about 9 min, NO reached a maximum concentration and decreased rapidly after that, to 30 to 50 nanomoles/litre after 15 min of ischemia. A decrease in the NO to ONOO- ratio correlated directly with an increase of myocardial infarction. After 15 min of ischemia, the cytoprotective effect of NO is diminished while the cytotoxic effect of ONOO- reached the maximum. ONOO- is the main product of nitroxidative stress. In the ischemic heart, a high concentration of ONOO- can trigger a chain of reactions leading to apoptosis, necrosis, and myocardial infarction.




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