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Gp91ds-Tat, A Selective Nadph Oxidase Peptide Inhibitor, Increases Blood Nitric Oxide (No) Bioavailability In Bind Limb Ischemia And Reperfusion (I/R), Sydney Walker, Tyler Galbreath, Qian Chen, Robert J. Barsotti, H. Patel, William Chau, Lindon H. Young
Gp91ds-Tat, A Selective Nadph Oxidase Peptide Inhibitor, Increases Blood Nitric Oxide (No) Bioavailability In Bind Limb Ischemia And Reperfusion (I/R), Sydney Walker, Tyler Galbreath, Qian Chen, Robert J. Barsotti, H. Patel, William Chau, Lindon H. Young
Research Day
I/R injury induces cell death and organ dysfunction in part due to a burst of reactive oxygen species that occurs upon the reintroduction of oxygen into the ischemic area, leading to endothelial dysfunction: decreased blood NO and increased hydrogen peroxide (H2O2 ) levels. We’ve previously shown in isolated rat hearts subjected to I/R injury, gp91ds-tat attenuated cardiac contractile dysfunction and reduced infarct size compared to controls presumably by the inhibition of NADPH oxidase induced superoxide release. Superoxide can quench NO via the formation of peroxynitrite and also be converted to H2O2 in blood. We attempted to confirm this hypothesis using …