Endothelial nitric oxide synthase (eNOS)-mediated production of NO regulates the microvasculature, controlling both vessel diameter and permeability. We hypothesized that T1 mapping of the healthy heart during NOS inhibition would detect increased water content resulting from increased coronary microvascular permeability, while a blunted change in T1 between baseline and NOS inhibition would indicate coronary eNOS dysfunction. Using these methods, we detected an increase in myocardial T1 of 113±15 ms due to NOS inhibition in control mice, but no change in eNOS-/- or HFD mice, demonstrating the eNOS mechanism and detection of coronary endothelial dysfunction in a model of heart disease.
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