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Ischemia-induced reactive hyperemia (RH) is mediated by various factors including release of nitric oxide (NO). The contribution of NO to RH equals the extent of L-NMMA-dependent reduction of forearm blood flow (FBF). Because the optimal duration and location of ischemia that provokes maximum NO activation is unknown, we analyzed which duration and location stimulates most NO release, aiming at developing a noninvasive tool to measure endothelial integrity by NO synthase activity in humans.

Nitric Oxide and Reactive Hyperemia: Role of Location and Duration of Ischemia