DMD TREATMENT: ANIMAL MODELS

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Duchenne muscular dystrophy (DMD) is characterized by the absence of dystrophin, which is accompanied by lack of sarcolemma localized neuronal nitric oxide synthase (nNOSμ). This lack of nNOS impairs the ability to blunt sympathetic vasoconstriction and may reduce local blood flow following muscle contractions. To compensate for lack of nNOSμ, treatments with phosphodiesters-5a (PDE5a) inhibitors have been proposed. In this study we utilized the post-contractile MRI blood-oxygenation-level-dependent (BOLD) response as an in vivo marker of skeletal muscle microvascular function to test the hypothesis that a PDE5a inhibitor (sildenafil citrate) improves muscle oxygenation after muscle contractions in mdx mice.

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